Seeking Real World Solutions to the Coronavirus Pandemic
News & Commentary Without Hysteria or Political Bias
New and Important! Updated July 28, 2020
- Two Big Pharma coronavirus vaccines begin the last phase of testing: 30,000-person trials, Washington Post
- Study says actual number of Covid-19 cases is far greater than thought, CNN
- Revealed: Seven year coronavirus trail from mine deaths to a Wuhan lab, Times of London (England)
- Nobel Laureate Calls COVID-19 Manmade, CNews (France)
- Russia First Nation to Finish Human Trials of Coronavirus Vaccine, Tass News Agency (Russia)
- Covid-19 Immunity May Rely on a Microscopic Helper: T Cells, Wired
- Do Not Fear the Coronavirus Wolf, by Bruce Brown
- Bruce Brown reviews the COVID-19 news coverage of the New York Times, Washington Post, CNN, etc.
- A Journal of the Plague Year by Daniel Defoe (1665): Then & Now
Index of Articles in chronological order
- What exactly is herd immunity?, MIT Technology Review, 3/17/2020
- Coronavirus Patients Betrayed by Their Own Immune System, New York Times, 4/1/2020
- COVID-19 is like three different diseases, says New York doctor, from flu-like illness to severe reactions and rare children’s syndrome, ABC News, 5/8/2020
- Your blood type could affect your risk from Covid-19, Advisory.com, 6/8/2020
- How the Coronavirus Short-Circuits the Immune System, New York Times, 6/11/2020
- Up to 96% of COVID-19 Infections May Be Asymptomatic, Science Daily, 6/12/2020
- Seattle Man Gets a $1.1 Million Coronavirus Hospital Bill, People, 6/15/2020
- Breaking down ‘miracle’ coronavirus survivor’s $1.1M hospital bill, New York Post, 6/17/2020
- Coronavirus death rate falling in hospitals, BBC, 6/26/2020
- Revealed: Seven year coronavirus trail from mine deaths to a Wuhan lab, Times of London, 7/4/2020
- Actual COVID-19 Death Rate Is About 1/2 of 1%, New York Times, 7/4/2020
- Coronavirus death rate keeps dropping even as alarm grows over summer surge, Washington Times, 7/6/2020
- Broadway Star Loses COVID-19 Battle, MedPage Today, 7/9/2020
- 68% of a New York clinic’s patients test positive for coronavirus antibodies, New York Times, 7/9/2020
- How coronavirus affects the entire body, CNN, 7/10/2020
- Covid-19 Immunity May Rely on a Microscopic Helper: T Cells, Wired, 7/10/2020
- Chinese virologist accuses Beijing of coronavirus cover-up, flees Hong Kong, FOX News, 7/10/2020
- 80% Of People Hospitalized With Coronavirus Still Had Symptoms Two Months Later, Forbes, 7/11/2020
- Florida’s 15,300 new COVID-19 cases sets a new U.S. pandemic record, South Florida Sun-Sentinal, 7/12/2020
- Russia first nation to finish human trials of Coronavirus vaccine, Tass News Agency, 7/12/2020
- Coronavirus: Could It Be Burning Out After 20 Percent of a Population Is Infected?, The Conversation / Umeå University, 7/12/2020
- A New Understanding of Herd Immunity, Atlantic Monthly, 7/13/2020
- Coronavirus warning from Italy: Effects of COVID-19 could be worse than first thought, Sky News, 7/13/2020
- Drugmakers will start coronavirus vaccine production by end of summer, Trump health officials say, CNBC, 7/13/2020
- Why a coronavirus vaccine won’t end the pandemic by itself, San Francisco Chronicle, 7/13/2020
- WHO: We won’t immediately have a ‘perfect vaccine,’ Business Insider, 7/13/2020
- CDC Director Pleads for Mask Compliance: If Everybody Wears One for Six Weeks, We Could Drive Covid ‘Into the Ground’, Mediaite.com, 7/13/2020
- World’s first recorded case of a child contracting COVID-19 from its mother inside the womb, Business Insider, 7/14/2020
- A Look at the Reinfection Rate, National Review, 7/14/2020
- Florida tops its single-day record for coronavirus deaths, but death rate falls through floor to less than 1%, 7/14/2020
- How a False Hydroxychloroquine Narrative Was Created, Mercola.com, 7/15/2020 (Commentary)
- Your Ancestors Knew Death in Ways You Never Will, New York Times, 7/15/2020 (Commentary)
- The coronavirus pandemic most resembles the 1957 Asian flu pandemic, Coronavirus Vaccine & Herd Immunity Digest, 7/16/2020
- Nobel Laureate Calls COVID-19 Manmade, CNews, 7/17/2020 (Commentary)
- State Department releases cable that launched claims that coronavirus escaped from Chinese lab, Washington Post, 7/18/2020 (Commentary)
- Study says actual number of Covid-19 cases is far greater than thought, CNN, 7/21/2020 (Commentary)
- Two Big Pharma coronavirus vaccines begin the last phase of testing: 30,000-person trials, Washington Post (Commentary)
According to the MIT Technology Review, when enough of the population is resistant to a germ, its spread stops naturally because not enough people are able to transmit it. Thus, the “herd” is immune, even though many individuals within it still are not.
Consider the Zika virus, a mosquito-borne illness that caused a epidemic panic in 2015 because of a link to birth abnormalities.
Two years later, in 2017, there was no longer nearly so much to worry about. A Brazilian study found by checking blood samples that 63% of the population in the northeastern beach city of Salvador had already had exposure to Zika; the researchers speculated that herd immunity had broken that outbreak.
Vaccines create herd immunity too, either when given widely or sometimes when administered in a “ring” around a new case of a rare infection. That’s how diseases like smallpox were eradicated and why polio is close to being erased. Various vaccine efforts are under way for this coronavirus, but they may not be ready for more than a year.
Even then, vaccine makers can find themselves in a losing race with nature to see which protects the herd first. That’s in part what happened in 2017, when drug maker Sanofi quietly abandoned a Zika vaccine in development after funding dried up: there simply wasn’t much of a market any longer.
For herd immunity to take hold, people must become resistant after they are infected. That occurs with many germs: people who are infected and recover become resistant to getting that disease again, because their immune system is charged with antibodies able to defeat it.
About 80,000 people have recovered from the coronavirus already, and it’s likely they are now resistant, although the degree of immunity remains unknown.
The point at which we reach herd immunity is mathematically related to the germ’s propensity to spread, expressed as its reproduction number, or R0. The R0 for the coronavirus is between 2 and 2.5, scientists estimate, meaning each infected person passes it to about two other people, absent measures to contain the contagion.
The current germ’s rate of spread is higher than that of the ordinary flu, but similar to that of novel emergent influenzas that have occasionally swept the globe before. “That is similar to pandemic flu of 1918, and it implies that the end of this epidemic is going to require nearly 50% of the population to be immune, either from a vaccine, which is not on the immediate horizon, or from natural infection,” according to Harvard University epidemiologist Marc Lipsitch.
The current epidemiological policies in most of the Western World now call for aggressive “suppression” of the virus by wearing face masks to limits the coronavirus’s spread, isolating sick people, and tracing their contacts.
However, there is an intrinsic downside to this approach.
“Suppressing transmission means that we won’t build up herd immunity,” says Azra Ghani, the lead epidemiologist on the new model of the outbreak from Imperial College London.
Ghani said the trade-off of success is “that we are driving it [herd immunity] down to such a low level that we have to keep those control [measures] in place.”
Commentary — the important take-away here is contained in the last two paragraphs, where Azra Ghani, epidemiologist at the Imperial College London, observes that the current “weak herd” approach being followed in the U.S. and much of the rest of the world is actually suppressing the very thing we desperately need right now, namely herd immunity to the coronavirus pandemic!
The “weak herd” approach also requires that economically devastating policies and totalitarian political controls be kept in place, permanently perhaps.
April 1, 2020 – The Coronavirus Patients Betrayed by Their Own Immune Systems, New York Times
The New York Times reports that a 42-year-old man arrived at a hospital in Paris on March 17 with a fever, cough and the “ground glass opacities” in both lungs that are a trademark of infection with the new coronavirus.
Two days later, his condition suddenly worsened and his oxygen levels dropped. His body, doctors suspected, was in the grip of a cytokine storm, a dangerous overreaction of the immune system. The phenomenon has become all too common in the coronavirus pandemic, but it is also pointing to potentially helpful drug treatments.
When the body first encounters a virus or a bacterium, the immune system ramps up and begins to fight the invader. The foot soldiers in this fight are molecules called cytokines that set off a cascade of signals to cells to marshal a response. Usually, the stronger this immune response, the stronger the chance of vanquishing the infection, which is partly why children and younger people are less vulnerable over all to coronavirus. And once the enemy is defeated, the immune system is hard-wired to shut itself off.
“For most people and most infections, that’s what happens,” said Dr. Randy Cron, an expert on cytokine storms at the University of Alabama at Birmingham.
But in some cases — as much as 15 percent of people battling any serious infection, according to Dr. Cron’s team — the immune system keeps raging long after the virus is no longer a threat. It continues to release cytokines that keep the body on an exhausting full alert. In their misguided bid to keep the body safe, these cytokines attack multiple organs including the lungs and liver, and may eventually lead to death.
In these people, it’s their body’s response, rather than the virus, that ultimately causes harm.
Cytokine storms can overtake people of any age, but some scientists believe that they may explain why healthy young people died during the 1918 pandemic and more recently during the SARS, MERS and H1N1 epidemics. They are also a complication of various autoimmune diseases like lupus and Still’s disease, a form of arthritis. And they may offer clues as to why otherwise healthy young people with coronavirus infection are succumbing to acute respiratory distress syndrome, a common consequence of a cytokine storm.
Reports from China and Italy have described young patients with clinical outcomes that seem consistent with this phenomenon. It’s very likely that some of these patients developed a cytokine storm, Dr. Cron said.
In the case of the 42-year-old patient, the suspected cytokine storm led his doctors to eventually try tocilizumab, a drug they have sometimes used to soothe an immune system in distress.
After just two doses of the drug, spaced eight hours apart, the patient’s fever rapidly disappeared, his oxygen levels rose and a chest scan showed his lungs clearing. The case report, described in an upcoming paper in Annals of Oncology, joins dozens of accounts from Italy and China, all indicating that tocilizumab might be an effective antidote to the coronavirus in some people.
On March 5, China approved the drug to treat serious cases of Covid-19, the disease caused by the coronavirus, and authorized clinical trials. On March 23, the U.S. Food and Drug Administration granted approval to the pharmaceutical company Roche to test the drug in hundreds of people with coronavirus infection.
Tocilizumab is approved to quieten the chatter of immune molecules in rheumatoid arthritis and in some types of cancer. It mutes the activity of a specific cytokine called interleukin-6 that is associated with an over-exuberant immune response.
“That’s the rationale for using the drug,” said Dr. Laurence Albiges, who cared for the patient at the Gustave Roussy Cancer Center in Paris.
May 8, 2020 – COVID-19 is like three different diseases, says New York doctor, from flu-like illness to severe reactions and rare children’s syndrome, ABC Net of Australia (Commentary)
ABC Net of Australia writes that almost 10 weeks into the pandemic, COVID-19 is continuing to surprise and baffle health experts.
In fact, experts’ picture of exactly how COVID-19 might play out in the body is now quite different to what was thought as little as a few weeks ago, with some experts saying it could be better described as three different diseases.
We have known for a while that the mild to moderate form of the disease — a flu-like illness with fever, muscle aches and respiratory symptoms, or often no symptoms at all — is almost like “child’s play” compared to the major damage to organs like the the lungs, heart, brain, and kidneys seen when COVID-19 becomes severe.
Umesh Gidwani, head of cardiac intensive care at New York’s Mount Sinai Hospital, says that trying to treat the severe form of the disease is like facing a terrifying fire, burning out of control.
“The patients we take care of [in intensive care] are those in whom the fire has already destroyed the house. But there continues to be embers and small fires. I can’t enter the house because it’s too hot and things are falling on me,” he says.
“[Severe disease] is almost a completely different animal [compared] to someone who is recovering at home with some chicken soup and paracetamol”.
And now it seems there is evidence of a third variation in illness that can occur following exposure to the virus — a mysterious new disease given the name paediatric multisystem inflammatory syndrome, with an entirely different set of symptoms again.
The syndrome seems to only affect children, unlike both mild and severe COVID-19, which mostly affect adults. However the link between the inflammatory syndrome and the virus that causes COVID-19 is not yet 100 per cent confirmed.
The bottom line, says Dr Gidwani, is what we have been calling a single disease — COVID-19 — is really looking more like three separate diseases.
He and others draw this conclusion based on how the virus affects the immune system.
“The key disaster is the extent and severity of the immune response,” he says.
It is now clear the symptoms experienced by people with severe COVID-19 are largely caused by the body’s disordered immune response to the virus rather than the virus itself, Dr Gidwani says.
In fact, the disordered immune response in severe COVID-19 is the disease; they are one and the same thing.
In contrast, with mild to moderate COVID, the immune response is more measured, with symptoms largely confined to the upper respiratory tract.
But with severe COVID-19, the body’s response to the infection goes into overdrive. In particular, substances called cytokines, which tell other parts of the immune system there is a problem that needs fixing in the body, and which coordinate the immune response, are released in excessive amounts.
This creates what’s known as a “cytokine storm”, which ends up causing damage to healthy tissue.
Doctors have seen similar cytokine storms in people with different kinds of infections or with certain cancers. But the cytokine storm with COVID-19 is wildly different.
As a result, therapies that work for the other cytokine storms don’t control the problem, Dr Gidwani says.
“My brain is thinking ‘what is going on? Is there a way to fix this?’ I don’t know what to do,” he says.
“It is very challenging, very frustrating, very upsetting.”
‘This is a brand new disease’
Understanding what makes the cytokine storm unique in severe COVID-19 is important as it means there may need to be a different approach to helping patients get better.
“This is a brand new disease. We are seeing more and more that the therapies we are used to working with don’t necessarily produce the same results with COVID,” Dr Gidwani says.
One important difference is that the cytokine storm in severe COVID-19 results in widespread blood clotting, which can in turn trigger heart attacks, strokes, deep vein thrombosis (DVT), pulmonary embolisms (clots in veins in the lungs) and limbs so damaged they may need to be amputated.
What’s more, Dr Gidwani says the surge in cytokines can last up to 45 days and can wax and wane. Patients may show an improvement, then a worsening — a pattern that can be repeated several times, often for weeks on end.
This can lead doctors to misjudge how sick a patient is and withdraw supportive measures such as a ventilator before they should.
“It is important to realise this is a distinct [immune] syndrome and that you can therefore avoid certain pitfalls,” says Dr Gidwani.
“This is not what we expected at the outset.
“But we never knew what to expect. I don’t know what will happen next either.”
Over-activation of the immune system could be a major “unifying element” that explains a large part of why the disease can play out in such different ways in severe COVID-19 and in PMIS, says Australian cardiologist and blood vessel researcher Jason Kovacic.
An immune attack on blood vessels potentially explains many of the key dangerous features of both conditions, says Dr Kovacic, who is Professor of Medicine and Cardiology both at New York’s Icahn School of Medicine and the Victor Chang Cardiac Research Institute at the University of NSW.
Rare mysterious illness in children
Paediatric multisystem inflammatory syndrome is an entirely different set of symptoms but it is nonetheless a “post-COVID-19” disease, Dr Gidwani says.
Symptoms may include fever, swollen hands and feet, a red rash that can occur on the skin around the lips and eyes, abdominal pain, diarrhoea and vomiting, resembling a rare condition called Kawasaki disease, thought to be triggered by infections.
But it is inflammation of the heart and blood vessels supplying it that make the condition potentially deadly.
Australian health authorities have pointed out the link between the syndrome and COVID-19 is unclear because not all affected children were positive in tests for current or past infection with the virus.
But it’s known “false negatives” — where no signs of current or past virus exposure are detected when that is not actually the case — can occur with these tests.
In all likelihood, the minority of cases who did not show a link with COVID-19 were in fact just undiagnosed cases because of inaccuracies with the tests, says Dr Gidwani.
Further investigation is underway to explore this idea.
The illness has appeared in 102 children from newborns to teenagers in the US in past two months, killing at least three.
Two of those died at Mount Sinai Hospital. Additional cases have been reported in the UK, Spain, France, Netherlands and Italy.
“All of these kids [with paediatric multisystem inflammatory syndrome] have some sort of inflammation of the blood vessels,” Dr Gidwani says.
“It is not due to the COVID itself but to an overblown immune reaction following COVID exposure.”
Immune attack may explain both conditions
In this sense, paediatric multisystem inflammatory syndrome seems similar to severe COVID-19, in that it is the result of a disordered immune response, triggered by the virus.
But the timing and nature of the immune response is different in the two conditions (with different outcomes in terms of symptoms).
In severe COVID-19, which occurs in about 10 per cent of patients, the immune over-activation usually occurs eight to 10 days after symptoms begin.
In the children’s syndrome, it seems the immune over-activation occurs either late in the course of infection, or after the virus has been cleared from the body.
“These kids have escaped the symptoms of the acute infection but they may not have escaped the post-infectious reaction to the virus.”
The condition is much rare than severe COVID, and it is thought that children who develop it may have unusual genetic vulnerabilities.
“Only a very small number of kids who get COVID exposure will get this,” Dr Giwani says.
“We do not have a good handle on what the number is but it’s pretty clear it is extremely rare.”
While treatments for the unique cytokine storm in COVID-19 are currently limited, recognising that it is new and different is nonetheless a vital first step towards tackling the problem and saving lives, Dr Kovacic says.
“It is a very, very, scary virus.”
Dr Gidwani agrees.
Australians should “thank God” they have not seen the devastation he has witnessed in New York.
“I do not wish it on anyone,” he says.
Commentary — This excellent story by ABC Net of Australia was one of the first to describe the many faces of COVID-19, which was initially thought to merely be “the flu on steroids.”
June 8, 2020 – Your blood type could affect your risk from Covid-19, Advisory.com
Advisory.com reports that researchers already have determined that a person’s age and whether they have certain underlying health conditions can affect their risk of developing a severe case of Covid-19, the disease caused by the new coronavirus. But now, some research suggests a person’s blood type may be another factor in whether they have a higher risk of developing a severe case of the disease.
For example, a preprint study published Tuesday that has not been peer-reviewed examined blood samples from 1,610 Covid-19 patients who developed severe cases of Covid-19, which the researchers classified as needing oxygen or a ventilator as part of their treatment. The researchers sequenced part of each those patients’ genomes, and then performed the same analysis on samples from 2,205 blood donors who did not have Covid-19 and compared the results.
The researchers found that many of the patients who had severe cases of Covid-19 possessed the same variant on a gene that determines a person’s blood type. Specifically, the researchers found that having blood type A was linked with a 50% increase in the likelihood a patient would develop a severe case of Covid-19.
According to the New York Times, a separate preprint study conducted by researchers in China that hasn’t yet been peer-reviewed found similar results. The study found that, out of 2,173 Covid-19 patients with different blood types, blood type A was associated with a higher risk of death from Covid-19 when compared with other blood types. The study also found that people with blood type A appeared more likely to contract the new coronavirus, whereas those with blood type O appeared to be the least likely to contract the virus.
Andre Franke, a molecular geneticist at the University of Kiel in Germany, who led the first study said he and his colleagues also identified another locus on Chromosome 3 that appeared to be linked with Covid-19. However, the researchers noted that locus hosts six different genes, and they’ve yet to determine which of those genes influences how Covid-19 develops.
Despite the findings, Franke said researchers are still unsure exactly how a person’s blood type plays a part in how Covid-19 affects them. “That is haunting me, quite honestly,” he said.
June 11, 2020 – How the Coronavirus Short-Circuits the Immune System, New York Times
The New York Times reports that at the beginning of the pandemic, the coronavirus looked to be another respiratory illness. But the virus has turned out to affect not just the lungs, but the kidneys, the heart and the circulatory system — even, somehow, our senses of smell and taste.
Now researchers have discovered yet another unpleasant surprise. In many patients hospitalized with the coronavirus, the immune system is threatened by a depletion of certain essential cells, suggesting eerie parallels with H.I.V.
The findings suggest that a popular treatment to tamp down the immune system in severely ill patients may help a few, but could harm many others. The research offers clues about why very few children get sick when they are infected, and hints that a cocktail of drugs may be needed to bring the coronavirus under control, as is the case with H.I.V.
Growing research points to “very complex immunological signatures of the virus,” said Dr. John Wherry, an immunologist at the University of Pennsylvania whose lab is taking a detailed look at the immune systems of Covid-19 patients.
In May, Dr. Wherry and his colleagues posted online a paper showing a range of immune system defects in severely ill patients, including a loss of virus-fighting T cells in parts of the body.
In a separate study, the investigators identified three patterns of immune defects, and concluded that T cells and B cells, which help orchestrate the immune response, were inactive in roughly 30 percent of the 71 Covid-19 patients they examined. None of the papers have yet been published or peer reviewed.
Researchers in China have reported a similar depletion of T cells in critically ill patients, Dr. Wherry noted. But the emerging data could be difficult to interpret, he said — “like a Rorschach test.”
Research with severely ill Covid-19 patients is fraught with difficulties, noted Dr. Carl June, an immunologist at the University of Pennsylvania who was not involved with the work.
“It is hard to separate the effects of simply being critically ill and in an I.C.U., which can cause havoc on your immune system,” he said. “What is missing is a control population infected with another severe virus, like influenza.”
That may create chaotic signaling in the body: “It’s like Usain Bolt hearing the starting gun and starting to run,” Dr. Hayday said, referring to the Olympic sprinter. “Then someone keeps firing the starting gun over and over. What would he do? He’d stop, confused and disoriented.”
The result is that the body may be signaling T cells almost at random, confusing the immune response. Some T cells are prepared to destroy the viruses but seem undermined, behaving aberrantly. Many T cells apparently die, and so the body’s reserves are depleted — particularly in those over age 40, in whom the thymus gland, the organ that generates new T cells, has become less efficient.
Some patients are severely affected by coronavirus infections because their immune systems respond too vigorously to the virus. The result, a so-called cytokine storm, also has been seen in cancer patients treated with drugs that supercharge T cells to attack tumors.
These overreactions can be quelled with medications that block a molecule called IL-6, another organizer of immune cells. But these drugs have not been markedly effective in most Covid-19 patients, and for good reason, Dr. Hayday said.
“There clearly are some patients where IL-6 is elevated, and so suppressing it may help,” he explained. But “the core goal should be to restore and resurrect the immune system, not suppress it.”
The new research may help answer another pressing question: Why is it so rare for a child to get sick from the coronavirus?
Children have highly active thymus glands, the source of new T cells. That may allow them to stay ahead of the virus, making new T cells faster than the virus can destroy them. In older adults, the thymus does not function as well.
The emerging picture indicates that the model for H.I.V. treatment, a cocktail of antiviral drugs, may be a good bet both for those with mild illnesses and those who are severely ill.
Some experts have wondered if antiviral treatment makes sense for severely ill Covid-19 patients, if their main affliction is an immune system overreaction.
But if the virus directly causes the immune system to malfunction, Dr. Hayday said, then an antiviral makes sense — and perhaps even more than one, since it’s important to stop the infection before it depletes T cells and harms other parts of the immune system.
“I have not lost one ounce of my optimism,” Dr. Hayday said. Even without a vaccine, he foresees Covid-19 becoming a manageable disease, controlled by drugs that act directly against the virus.
“A vaccine would be great,” he said. “But with the logistics of its global rollout being so challenging, it’s comforting to think we may not depend on one.”
June 12, 2020 — Up to 96% of COVID-19 Infections May Be Asymptomatic, Science Daily (Commentary)
Science Daily reports that many — if not most — people who are infected with the coronavirus don’t feel bad or get sick. In fact, they feel completely normal and don’t even know they have the supposedly dread virus!
The headline on the June 12 Science Daily story actually reads “Up to 45 percent of SARS-CoV-2 infections may be asymptomatic,” but when you read the story you find that asymptomatic COVID-19 infections may actually be as high as 96 percent of total COVID-19 infections.
“Among more than 3,000 prison inmates in four states who tested positive for the coronavirus, the figure was astronomical: 96 percent asymptomatic.”
In other words, most and maybe nearly all of the people infected with the COVID-19 virus don’t get sick!
The Science Daily story was based on data from the Scripps Research Institute published in Annals of Internal Medicine.
Commentary — It is undeniably excellent news that most people who are infected with COVID-19 don’t get sick, but like so much COVID-19 press coverage, Science Daily sees this very good news casting a horrific shadow because asymptomatic COVID-19 carriers may infect others.
June 15, 2020 – Seattle Man Gets a $1.1 Million Bill After Spending 62 Days in the Hospital with Coronavirus, People Magazine (Commentary)
People Magazine writes that a Seattle man who spent 62 days in the hospital with a near-deadly case of COVID-19 had a “heart-stopping” moment when he received the bill, for $1.1 million.
Michael Flor, 70, had a severe case of COVID-19, the Seattle Times reported. He spent most of those 62 days at Swedish Medical Center in Issaquah, Washington in a sealed room in the intensive care unit to protect others at the hospital, and 29 days on a ventilator. His heart, kidneys and liver were all failing at points during his stay, and at one point he was so close to dying that a nurse held a phone up to his ear so his wife and kids could say their last goodbyes.
But Flor recovered, and finally went home at the beginning of May. Seeing his hospital bill, though, was a shock.
“I opened it and said ‘holy [bleep]!’ ” he told the Times.
The 181-page hospital bill includes a day fee of $9,736 — $408,912 total — for his ICU room, around a quarter of a million for the various drugs doctors tried on him and $82,215 for the ventilator he used for 29 days. In all, the bill was for $1,122,501.04, and includes almost 3,000 itemized charges.
Flor also thinks more bills are on the way for the two weeks he spent in a rehabilitation center, his dialysis treatments and for the doctors’ labor.
Thankfully, Flor most likely will not have to pay any of it. He has Medicare and Medicare Advantage insurance through Kaiser Permanente, which would cover the bulk of the bill. The company has said that they will waive most out-of-pocket costs for COVID-19 treatment in 2020 thanks to the $100 billion emergency funding bill from Congress, meaning he likely won’t have to pull together his estimated $6,000 co-pay.
Flor also feels guilty that he has good health insurance when other Americans do not, and he also recognizes that thanks to the funding bill, his hospital stay is paid for from taxpayer money and insurance money from people with non-COVID-19 bills.
“It was a million bucks to save my life, and of course I’d say that’s money well-spent,” he says. “But I also know I might be the only one saying that.”
Commentary — Based on the press coverage of this incident, I would say that Michael Flor appears to be an intelligent and caring man. But just as clearly, I would say he should NOT have been saved. This is a ludicrous waste of public and private health care resources!
Coronovirus is a wolf come to cleanse our sad and sick species of the weak and the elderly, and make humanity strong again. If we persist in this insane course of action, humanity will perish. It’s sad when a good man has to die, but it’s more important that a strong and resilient human species live on!
June 17, 2020 – Breaking down ‘miracle’ coronavirus survivor’s $1.1M hospital bill, New York Post (Commentary)
The New York Post writes that a Seattle COVID-19 survivor knew that he must have run up a pretty huge medical tab after spending March and April in the hospital, including more than a month in the intensive care unit. But Michael Flor, 70, told the Seattle Times that the 181-page, $1.1 million hospital bill nearly gave him a heart attack.
“I opened it and said ‘Holy [bleep]!’” he said.
Flor was dubbed “the miracle child” by nurses at Swedish Medical Center in Issaquah, Wash., for his incredible turnaround after spending four weeks on a ventilator. He was so close to death at one point that a night-shift nurse held a phone to his ear so that his wife and children could say their final goodbyes from quarantine. He was “as sick as you can get, with basically every organ system shutting down,” according to one of his doctors.
The good news is that Flor recovered and is back at home. And he’s probably off the hook for that $1.1 million, because his insurance is footing the bill for most of his medical costs. And his remaining $6,000 out-of-pocket expenses will probably be picked up by the more than $100 billion that Congress has earmarked to help hospitals and insurance companies cover the costs of the COVID-19 pandemic. But Flor’s hospital bill still offers a fascinating look at the cost of treating a life-threatening illness such as COVID-19.
Here’s how the $1,122,501.04 bill breaks down:
The 181-page book — sorry, bill — includes almost 3,000 itemized charges, averaging about 50 a day. The greatest expense by far was his 42-day stay in the ICU, totaling $408,912. His room had to be sealed, and was accessed only by medical staff wearing plastic suits and headgear, which cost $9,736 a day.
Flor also was hooked to a mechanical ventilator for 29 days, which at $2,835 a day ran up to $82,215.
There were two days when his heart, kidneys and lungs were all failing. And the bill for that touch-and-go period spans 20 pages and runs almost $100,000 in costs as doctors “were throwing everything at me they could think of,” Flor said.
Almost a quarter of the bill includes various drug costs, and this accounting doesn’t even factor in Flor’s two weeks of recovery in a rehabilitation facility.
Flor said that the bill has given him survivor’s guilt. “There’s a sense of ‘why me?’ Why did I deserve all this?” he told the Seattle Times. “Looking at the incredible cost of it all definitely adds to that survivor’s guilt.”
But he should know that he’s not the only COVID-19 survivor to be shocked with a surprise medical bill following a bout with the deadly disease that’s killed 116,250 Americans and counting. Lawyer turned writer David Lat recently wrote about his own $320,000 COVID-19 bill in Slate. He spent 16 nights in the hospital in March, including a week in the ICU and six days on a ventilator.
And while he was bracing to pay $6,000 or $7,000 in out-of-pocket costs, he also didn’t end up on the hook for any of it because his hospital, NYU Langone, was in-network for his insurance company, UnitedHealthcare. And UHC is among the insurance companies that have waived patient cost-sharing for COVID-19 treatment.
But this doesn’t mean that everyone can expect “free” coronavirus treatment. While the nation’s largest insurers, including Aetna CVS, Anthem, Blue Cross Blue Shield, Cigna, Humana and United Healthcare, did announce that they are not making patients pay deductibles, copays, coinsurance and other charges if they are hospitalized with COVID-19, the people who get health insurance through their jobs may still end up having to pay for treatment. And that’s because employers with “self-funded” or “self-insured” health plans are allowed to opt out of waiving cost-sharing for their employees. What’s more, insurers are only waiving this cost-sharing for a limited time.
The City University of New York (CUNY) Graduate School of Public Health and Health Policy recently ran a computer simulation to gauge what the nation’s COVID-19-related health care costs could be. They determined that the median cost of a coronavirus hospitalization is $14,366. And that doesn’t include the long-term health care costs for patients with severe illness who suffer significant lung damage, for example. Other estimates have pushed COVID-19 hospitalization costs closer to $20,000.
Even COVID-19 testing, which is supposed to be free, has resulted in some eye-watering bills. Earlier in the pandemic, a Miami man reportedly racked up $3,270 in hospital charges when he went in for a COVID-19 test after a work trip to China. And a Pennsylvania man had to set up a GoFundMe page to help pay for $3,918 in surprise bills after he was evacuated from China and quarantined with his 3-year-old daughter.
Indeed, Flor’s bill and these other COVID-19 hospital costs are a stark reminder that: one in six Americans get hit with a “surprise” medical bill after a trip to the emergency room; one in five Americans get hit with a surprise medical bill after elective surgery; and one in five patients hospitalized with a severe case of pneumonia get stuck with a surprise medical bill from an out-of-network provider. What’s more, the American Cancer Society estimates that 137 million Americans are burdened by medical debt — and cancer treatment is a huge part of that, of course, with one in four cancer survivors struggling to pay medical bills.
Flor added that while he feels that a million bucks to save his life is “money well-spent,” he also appreciates that “I might be the only one saying that.”
Commentary — Can you handle a little blunt truth? We can not afford this sort of counter-productive folly. It is important that COVID-19 kill the weak, both to contain the spread of the disease, and to strengthen the human species, or “herd.” Saving the weak at immense expense is lunacy. As the country western song says, “the secret to a long life is knowning when it’s time to go.”
June 26, 2020 – Coronavirus death rate falling in hospitals, BBC
University of Oxford researchers found the proportion of coronavirus patients dying each day in England fell from 6% to 1.5% between April and June.
Improvements in treatments, changes in the patient population and seasonal effects could all play a role.
The data emerged as the government prepares to ease lockdown restrictions.
Around the height of the outbreak, on 8 April, there were 15,468 people in hospital in England with coronavirus of whom 899 died (6%).
By 21 June there were 2,698 hospitalized coronavirus patients, 30 of whom died (1%), according to the most recent data compiled University of Oxford’s Centre for Evidence-Based Medicine.
Hospital case fatality is a measure used since the beginning of the outbreak, providing consistent figures and enabling researchers to look for trends.
Commentary — this is dramatic and excellent news on the direst part of the coronavirus pandemic! And it has been followed by similar declines in coronavirus-caused deaths in the United States as well.
July 4, 2020 – Revealed: Seven year coronavirus trail from mine deaths to a Wuhan lab, Times of London (Commentary)
The Times of London writes that in the monsoon season of August 2012 a small team of scientists travelled to southwest China to investigate a new and mysteriously lethal illness. After driving through terraced tea plantations, they reached their destination: an abandoned copper mine where — in white hazmat suits and respirator masks — they ventured into the darkness.
Instantly, they were struck by the stench. Overhead, bats roosted. Underfoot, rats and shrews scurried through thick layers of their droppings. It was a breeding ground for mutated micro-organisms and pathogens deadly to human beings. There was a reason to take extra care. Weeks earlier, six men who had entered the mine had been struck down by an illness that caused an uncontrollable pneumonia. Three of them died.
Today, as deaths from the Covid-19 pandemic exceed half a million and economies totter, the bats’ repellent lair has taken on global significance.
Evidence seen by The Sunday Times suggests that a virus found in its depths — part of a faecal sample that was frozen and sent to a Chinese laboratory for analysis and storage — is the closest known match to the virus that causes Covid-19.
It came from one of the last droppings collected in the year-long quest, during which the six researchers sent hundreds of samples back to their home city of Wuhan. There, experts on bat viruses were trying to identify the source of the Sars — severe acute respiratory syndrome — pandemic 10 years earlier.
The virus was a huge discovery. It was a “new strain” of a Sars-type coronavirus that, surprisingly, received only a passing mention in an academic paper. The six sick men were not referred to at all.
What happened to the virus in the years between its discovery and the eruption of Covid-19? Why was its existence tucked away in obscure records, and its link to three deaths not mentioned?
Nobody can deny the bravery of the scientists who risked their lives by harvesting the highly infectious virus. But did their courageous detective work lead inadvertently to a global disaster?
Where flowers bloom all year – The first victims of a new virus
Kunming, the capital of Yunnan province in southwest China, is known as “the city of eternal spring” because its unique climate encourages flowers to bloom all year. The sprawling high-rise buildings of the First Affiliated Hospital tower over the ancient city.
On Tuesday April 24, 2012, a 45-year-old man with the surname of Guo was admitted to the hospital’s intensive care unit suffering from severe pneumonia.
The next day a 42-year-old man with the surname Lv was taken to the hospital with the same life-threatening symptoms, and by Thursday three more cases — Zhou, 63, Liu, 46, and Li, 32 — had joined him in intensive care. A sixth man called Wu, 30, was taken into intensive care the following Wednesday.
All the men were linked. They had been given the task of clearing out piles of bat faeces in an abandoned copper mine in the hills south of the town of Tongguan in the Mojiang region. Some had worked for two weeks before falling ill, and others just a few days.
The illness confounded the doctors. The men had raging fevers of above 39C, coughs and aching limbs. All but one had severe difficulty in breathing.
After the first two men died, the remaining four underwent a barrage of tests for haemorrhagic fever, dengue fever, Japanese encephalitis and influenza, but they all came back negative. They were also tested for Sars, the outbreak that had erupted in southern China in 2002, but that also proved negative.
The doctors sought the opinion of Professor Zhong Nanshan, a British-educated respiratory specialist and a former president of China’s medical association who had spearheaded his country’s efforts to combat Sars. Aware the men might be suffering from another Sars-related coronavirus, he advised the doctors to test them for antibodies.
The Wuhan Institute of Virology (WIV), a renowned centre of coronavirus expertise, was called in to test the four survivors. These produced a remarkable finding: while none had tested positive for Sars, all four had antibodies against another, unknown Sars-like coronavirus.
Furthermore, two patients who recovered and went home showed greater levels of antibodies than two still in hospital, one of whom later died.
Researchers in China have been unable to find any news reports of this new Sars-like coronavirus and the three deaths. There appears to have been a media blackout. It is, however, possible to piece together what happened in the Kunming hospital from a master’s thesis by a young medic called Li Xu. His supervisor was Professor Qian Chuanyun, who worked in the emergency department that treated the men. Other vital details, including the results of the antibody tests, were found in a PhD paper by a student of the director of the Chinese Centre for Disease Control and Prevention.
Li’s thesis was unable to say what exactly killed the three miners, but indicated that the most likely cause was a Sars-like coronavirus from a bat.
“This makes the research of the bats in the mine where the six miners worked and later suffered from severe pneumonia caused by unknown virus a significant research topic,” Li concluded.
That research was already under way — led by the Wuhan virologist who became known as “Bat Woman” — and it adds to the mystery.
The Bat Heroine – The Bat Woman heralded as a hero in China
For historians of the Chinese Communist Party, Wuhan is where the 72-year-old Mao Tse-tung took a symbolic swim in the Yangtze River in 1966 before launching the Cultural Revolution. For generations born since that disastrous era, the modern industrial city is the crossroads of China’s high-speed rail network and was the centre of the Covid-19 pandemic.
For science, however, Wuhan is the centre for research into the coronavirus in bats. Shi Zhengli, nicknamed “Bat Woman” by her colleagues, is heralded as a hero in China and in scientific communities across the world.
But the bats in Yunnan are 1,000 miles from her laboratory, and one of the most extraordinary coincidences of the Covid-19 pandemic is that ground zero happened to be in Wuhan, the world centre for the study and storage of the types of coronavirus the city’s own scientists believe caused the outbreak.
Coronaviruses are a group of pathogens that sometimes have the potential to leap species from animals to humans and appear to have a crown — or corona — of spikes when viewed under a microscope.
Before Covid-19, six types of coronavirus were known to infect humans but mostly they caused mild respiratory symptoms such as the common cold.
The first outbreak of Sars — now known as Sars-Cov-1 to distinguish it from Sars-Cov-2, the virus that causes Covid-19 — is one of the deadly exceptions. It emerged in Guangdong, southern China, in November 2002 and infected 8,096 people in 29 countries. It caused severe pneumonia in some and killed 774 people before petering out eight months later.
A race began to find out how a coronavirus had mutated into something so deadly and jumped from animals to humans. The initial prime suspects were masked palm civet cats, a delicacy in some parts of China. But suspicion shifted to bats, which had also been linked to other deadly viruses such as rabies. Perhaps they were the primary source and civets were just intermediaries that they infected.
Shi and her team from the WIV began hunting among bat colonies in caves in southern China in 2004. In 2012 they were in the midst of a five-year research project centred on caves in remote mountains southwest of Kunming when the call came to investigate the incident in the copper mine about 200 miles away.
They were joined by local disease control experts when they descended into the mine that August with protective equipment and bat-catching nets.
Over the next year, the scientists took faecal samples from 276 bats. The samples were stored at minus 80C in a special solution and dispatched to the Wuhan institute, where molecular studies and analysis were conducted.
These showed that exactly half the bats carried coronaviruses and several were carrying more than one virus at a time — with the potential to cause a dangerous new mix of pathogens.
The results were reported in a scientific paper entitled “Coexistence of multiple coronaviruses in several bat colonies in an abandoned mineshaft” co-authored by Shi and her fellow scientists in 2016.
Notably, the paper makes no mention of why the study had been carried out: the miners, their pneumonia and the deaths of three of them.
The paper does state, however, that of the 152 genetic sequences of coronavirus found in the six species of bats in the mineshaft, two were of the type that had caused Sars. One is classified as a “new strain” of Sars and labelled RaBtCoV/4991. It was found in a Rhinolophus affinis, commonly known as a horseshoe bat. The towering significance of RaBtCov/4991 would not be fully understood for seven years.
An ordinary coronavirus – The top security lab at the centre of Wuhan
A new facility was taking shape on the virology institute campus on the west side of the Yangtze in Wuhan. Built by a contractor for the People’s Liberation Army under strict secrecy, a top-security laboratory for handling deadly human pathogens was unveiled in 2017.
There were 31 such laboratories in the world at the time but this was China’s first. The new lab had been certified by the Chinese authorities as “biosafety level 4”, or BSL-4, the highest. But it was raising eyebrows internationally.
Scientists and biosafety experts were concerned that the closed nature of the Chinese state and the emphasis on hierarchy would prove incompatible with running such a dangerous facility.
“Diversity of viewpoint, flat structures where everyone feels free to speak up and openness of information are important,” Tim Trevan, a consultant in biosecurity, told the science magazine Nature when it opened.
Laboratory leaks are not uncommon. In the past, ebola and the fatal bat disease Marburg, which kills nine out of 10 people infected, have escaped from BSL-4 laboratories in the US. American health authorities recorded 749 laboratory safety breaches in the six years to 2015. Indeed, several people were infected by Sars in 2004 after an accident at China’s National Institute of Virology in Beijing.
The need for a secure facility in Wuhan was obvious, however. Shi and her team had already collected hundreds of samples of the coronavirus — including RaBtCov/4991 — from their work on bats across Yunnan province, and they were running controversial experiments to find out how they might mutate to become more infectious to humans.
This “gain-of-function” work is described in papers released by the WIV between 2015 and 2017, scientists say. Shi’s team combined snippets of different coronaviruses to see if they could be made more transmissible in what they called “virus infectivity experiments”.
It was controversial because it had the potential to turn bat coronaviruses into human pathogens capable of causing a pandemic. In 2014 the US government issued a ban on funding any endeavour to make a virus more contagious.
Shi’s team argued that gain-of-function work increased its understanding of how an ordinary coronavirus might one day transform into a killer such as Sars.
Others disagreed. “The debate is whether in fact you learn more by helping to develop vaccines or even drugs by replicating a more virulent virus than currently exists, versus not doing that,” explained Deenan Pillay, professor of virology at University College London. “And I think the consensus became that the risk was too much.”
In January 2018 the US embassy in Beijing took the unusual step of sending scientists with diplomatic status to Wuhan to find out what was going on in the institute’s new biosafety laboratories. They met Shi and members of her team.
Details of the diplomats’ findings have been found in US diplomatic cables that were leaked to the Washington Post and others. “Most importantly,” states a cable from January 19, 2018, “the researchers also showed that various Sars-like coronaviruses can interact with ACE2, the human receptor identified for Sars-coronavirus. This finding strongly suggests that Sars-like coronaviruses from bats can be transmitted to humans to cause Sars-like diseases.”
The Americans were evidently worried about safety. “During interactions with scientists at the WIV laboratory, they noted the new lab has a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory,” the cable added.
Shi was in a conference in Shanghai on Monday December 30, 2019, when she received a call to say there was a new coronavirus on the loose — and it had surfaced in Wuhan, of all places. Since her work had established that such viruses were most likely to originate in south China, she found the news puzzling and extremely worrying. “I wondered if [the local health authority] got it wrong,” she told the Scientific American magazine in a rare interview this year. “I had never expected this kind of thing to happen in Wuhan, in central China.”
One of her initial thoughts, as she prepared to return immediately to analyse the virus, was “Could they [the new coronaviruses] have come from our lab?”. It was a natural anxiety, although she said she was later able to dismiss it after examining the lab’s records.
Patient Zero – When did Covid-19 really start?
The precise point at which Covid-19 erupted in Wuhan may never be known. Various theories have been discredited.
A study by Harvard University claimed the virus may have started last August. It relied on satellite images in which the car parks of selected Wuhan hospitals looked busier. However, the study’s detractors have pointed to discrepancies in the evidence.
There is also a theory — propagated by the Chinese media — that the virus may have been introduced into the country by foreign athletes competing in the Military World Games in Wuhan last October. They included the French former world champion pentathlete Élodie Clouvel and the Italian Olympic gold medallist fencer Matteo Tagliariol, who were laid low by fever during the Games.
Few of the athletes have been tested to find out whether they carry antibodies to Covid-19, apart from the Swedish team. Melina Westerberg, a Swedish pentathlete, has revealed that while many of her teammates were sick during the Games, they tested negative. “It was just a coincidence,” she said.
It is possible that the virus did start patchily at around the time of the Military World Games. Yu Chuanhua, an epidemiology professor at Wuhan University, has told Chinese media that one man was admitted to hospital on September 29 with Covid-19-like symptoms but it is impossible now to show whether he had the virus because he died. There were two more suspected early carriers of the virus from November 14 and 21 in the city’s 47,000-strong database of cases, but they are unconfirmed.
Probably the first confirmed case was a 70-year-old man with Alzheimer’s disease, whose family had told researchers from Wuhan Jinyintan Hospital that his symptoms had begun on December 1.
From that point it accelerated to about 60 identifiable cases by December 20, according to government research data reported in the South China Morning Post. However, it would not be until a week later that Dr Zhang Jixian, of the Hospital of Integrated Traditional Chinese and Western Medicine in Hubei province, became the first person to report a suspected outbreak to the provincial government.
By then it had already spread as far as Europe, probably via regular flights from Wuhan. The virus may have been in Italy as early as December 18. The country’s National Institute of Health reported finding traces of Covid-19 in sewage water collected in Milan and Turin on that date.
It was certainly in France, as a man called Amirouche Hammar was admitted to Jean-Verdier hospital in Paris on December 27. He had unknown respiratory pneumonia and was coughing blood. His samples later revealed Covid-19. His wife, who had a slight cough, worked at a supermarket used by shoppers leaving Charles de Gaulle airport, where there were direct flights from Wuhan.
In Wuhan itself, the first cluster of cases included traders and shoppers at the Huanan seafood market, a maze of small trading stores opening on to crowded alleys in the centre of the city. Despite its name, the market also sold meat and vegetables, and there was an exotic wildlife section in the west of the market.
On January 1 the Huanan market was closed and scientists found 33 coronavirus samples, nearly all in the area of the market where wild animals were sold.
It seemed like an open and shut case. When the results were released later that month, the Chinese state news agency Xinhua reported: “The results suggest that the novel coronavirus outbreak is highly relevant to the trading of wild animals.”
However, an early study published in The Lancet made clear that of the 41 patients who contracted Covid-19 in Wuhan only 27 had been “exposed” to the market. A third had no connection to the market, including the study’s “patient zero”, who fell ill on December 1.
Months later George Gao, the director of the Chinese Centre for Disease Control and Prevention, revealed that all the samples taken from animals at the market had tested negative for the virus and that those found had been from sewage or other environmental sources. The Chinese health authorities are now working on the theory that the market helped spread the disease but was not where it originated.
Mapping the virus – China warns world of deadly new strain
On December 31, the day Shi returned to the WIV to begin work identifying the new coronavirus, the Chinese authorities decided it was time to tell the world there was potentially a problem.
The World Health Organisation (WHO) was notified that a number of people had been struck down with pneumonia but the cause was not stated. On the same day, the Wuhan health authority put out a bland public statement reporting 27 cases of flu-like infection and urged people to seek medical attention if they fell ill. Neither statement indicated that the new illness could be transmitted between humans or that the likely source was already known: a coronavirus.
By the second week in January, desperate scenes were unfolding at Wuhan hospitals. Hopelessly ill-prepared and ill-equipped staff were forced to make life-and-death calls about who they could treat. Within a few days, the lack of beds, equipment and staff made the decisions for them.
Shi’s team managed to identify five cases of the coronavirus from samples taken from patients at Wuhan Jinyintan Hospital using a technique to amplify the virus’s genetic material. The samples were sent to another lab, which completed the whole genomic sequence.
However, the sequence would not be passed to the WHO until January 12 and China would not admit there had been human-to-human transmission until January 20, despite sitting on evidence the virus had been passed to medics.
One of Shi’s other urgent tasks was to check through her laboratory’s records to see if any errors, particularly with disposal of hazardous materials, could have caused a leak from the premises.
She spoke of her relief to discover that the sequences for the new virus were not an exact match with the samples her team had brought back from the bat caves. “That really took a load off my mind,” she told Scientific American, “I had not slept a wink for days.”
RaTG13 – From bat cave to lab
She then set about writing a paper describing the new coronavirus to the world for the first time. Published in Nature on February 3 and entitled “A pneumonia outbreak associated with a new coronavirus of probable bat origin”, the document was groundbreaking.
It set out a full genomic description of the Covid-19 virus and revealed that the WIV had in storage the closest known relative of the virus, which it had taken from a bat. The sample was named RaTG13. According to the paper, it is a 96.2% match to the Covid-19 virus and they share a common lineage distinct from other Sars-type coronaviruses. The paper concludes that this close likeness “provides evidence” that Covid-19 “may have originated in bats”.
In other words, RaTG13 was the biggest lead available as to the origin of Covid-19. It was therefore surprising that the paper gave only scant detail about the history of the virus sample, stating merely that it was taken from a Rhinolophus affinis bat in Yunnan province in 2013 — hence the “Ra” and the 13.
Inquiries have established, however, that RaTG13 is almost certainly the coronavirus discovered in the abandoned mine in 2013, which had been named RaBtCoV/4991 in the institute’s earlier scientific paper. For some reason, Shi and her team appear to have renamed it.
The clearest evidence is in a database of bat viruses published by the Chinese Academy of Sciences — the parent body of the WIV — which lists RaTG13 and the mine sample as the same entity. It says it was discovered on July 24, 2013, as part of a collection of coronaviruses that were described in the 2016 paper on the abandoned mine.
In fact, researchers in India and Austria have compared the partial genome of the mine sample that was published in the 2016 paper and found it is a 100% match with the same sequence for RaTG13. The same partial sequence for the mine sample is a 98.7% match with the Covid-19 virus.
Peter Daszak, a close collaborator with the Wuhan institute, who has worked with Shi’s team hunting down viruses for 15 years, has confirmed to The Sunday Times that RaTG13 was the sample found in the mine. He said there was no significance in the renaming. “The conspiracy folks are saying there’s something suspicious about the change in name, but the world has changed in six years — the coding system has changed,” he said.
He recalled: “It was just one of the 16,000 bats we sampled. It was a faecal sample, we put it in a tube, put it in liquid nitrogen, took it back to the lab. We sequenced a short fragment.”
In 2013 the Wuhan team had run the sample through a polymerase chain reaction process to amplify the amount of genetic material so it could be studied, Daszak said. But it did no more work on it until the Covid-19 outbreak because it had not been a close match to Sars.
Other scientists find the initial indifference about a new strain of the coronavirus hard to understand. Nikolai Petrovsky, professor of medicine at Flinders University in Adelaide, South Australia, said it was “simply not credible” that the WIV would have failed to carry out any further analysis on RaBtCoV/4991, especially as it had been linked to the deaths of three miners.
“If you really thought you had a novel virus that had caused an outbreak that killed humans then there is nothing you wouldn’t do — given that was their whole reason for being [there] — to get to the bottom of that, even if that meant exhausting the sample and then going back to get more,” he said.
“I would expect people to be as clear as they can be about the history of the isolates of their sequencing,” said Professor Wendy Barclay, head of Imperial College London’s infectious disease department and a member of the UK government’s Sage advisory committee. “Most of us would have reported the entire history of the isolate, [back] to where all that came from, at the time.”
According to Daszak, the mine sample had been stored in Wuhan for six years. Its scientists “went back to that sample in 2020, in early January or maybe even at the end of last year, I don’t know. They tried to get full genome sequencing, which is important to find out the whole diversity of the viral genome.”
However, after sequencing the full genome for RaTG13 the lab’s sample of the virus disintegrated, he said. “I think they tried to culture it but they were unable to, so that sample, I think, has gone.”
In recent weeks, academics are said to have written to Nature asking for the WIV to write an erratum clarifying the sample’s provenance, but the Chinese lab has maintained a stony silence. A spokesman for Nature said: “Concerns relating to this paper have been brought to Nature’s attention and are being considered at the moment. We cannot comment further at this time.”
Ski holiday – The contagion spread through Europe
The director of the WIV, Wang Yanyi, gave an interview in May in which she described suggestions that Covid-19 might have leaked from the lab as “pure fabrication”. She said that the institute managed to sequence the genome of RaTG13 but had not been able to return it to a live virus. “Thus, there is no possibility of us leaking RaTG13,” she said.
Shi’s interview with the Scientific American mentions the discovery of a coronavirus that 96% matches the Covid-19 virus, and has a reference to the miners dying in a cave she investigated. However, the two things are not linked and Shi downplays the significance of the miners’ deaths by claiming they succumbed to a fungus.
Experts consulted by this newspaper thought it was significant the men had tested positive for antibodies against Sars. Professor Martin Hibberd, a professor of emerging infectious diseases at the London School of Hygiene & Tropical Medicine, said the antibodies provided “a good clue” that the cause of death was “a proper coronavirus”, which “most likely” was Sars-related.
“[RaTG13] is so similar to all the other Sars coronaviruses and so I’d imagine all of that family can cause similar disease, so it makes good sense to me that if the miners caught it they would end up with something that looks similar.”
On January 23 Wuhan became the first city in the world to go into lockdown and it would later suffer nearly 4,000 deaths, according to official figures that some people believe are too low.
Britain’s first official cases — a Chinese student studying in York and a relative — would not emerge for another week, but it is highly likely the virus was already in the country. There were 901 flights from China to the UK between December 1, when the first known patient fell ill, and January 24. Of those, 23 flights brought thousands of passengers directly from Wuhan to Heathrow.
There is also evidence that Britons were bringing back the virus from Europe. Professor Tim Spector, an epidemiologist at King’s College London, who runs the Covid Symptom Study app, says he was contacted by up to 500 people who had returned to the UK between Christmas and January with symptoms.
Many were returning from ski resorts, notably in Austria. In April, 42% of residents in the town of Ischgl were found to have antibodies. “I was interested in the Austrian surveys done in Tyrol because I was quite struck by the stories of all the people that came back from Austrian ski holidays in January, predominantly, feeling ill. It was very convincing because a lot of the stories were the same from different people,” he said.
The investigation – How did this happen?
The origin of Covid-19 is one of the most pressing questions facing humanity. Scientists worldwide are trying to understand how it evolved, which could help stop such a crisis happening again.
The suggestion that well-intentioned scientists may have introduced Covid-19 to their own city is vehemently denied by the WIV, and its work on the origin of the virus has become an x-rated topic in China. Its leadership has taken strict control of new studies and information about where the virus may have come from.
A directive from the education ministry’s science and technology department in the spring stipulated that such work had to be read by a taskforce directly under the state council — comprising China’s president, Xi Jinping, and top ministers — before it can be published.
The secrecy has only increased as the origin of Covid-19 has become politicised as a weapon of aggressive foreign policy. President Donald Trump has described the virus as a “kung flu” and has delighted in claiming it is a Chinese disease. Scientists are dismayed and fear China will retreat further into its shell.
Professor Richard Ebright, of Rutgers University’s Waksman Institute of Microbiology in New Jersey, believes there is now less than a 50:50 chance China will allow a transparent investigation into the origin of the pandemic. “That’s unfortunate,” he said. “And that largely reflects the poor handling of the matter by the US president, who chose to push this in a way that made it unlikely that there could be an open investigation.”
Over the next few days, WHO scientists will be allowed to fly into China to begin an investigation into the origins of the virus after two months of negotiations. Many experts such as Daszak believe the source of the virus will be found in a bat in the south of China.
“It didn’t emerge in the market, it emerged somewhere else,” said Daszak. He said the “best guess right now” is that the virus started within a “cluster” on the Chinese border that includes the area where RaTG13 was found and an area just south of the mineshaft, where another bat pathogen with a 93% likeness to Covid-19 was discovered recently.
As for how the virus travelled to Wuhan, Daszak said: “Fair assumption is that it spilt into animals in southern China and was then shipped in, via infected people, or animals associated with trade, to Wuhan.”
But how could such an infectious virus avoid causing a single noticeable outbreak during the 1,000-mile journey from Yunnan to the city?
Hibberd said it was feasible the virus could have travelled in an animal such as a pangolin, which passed it to a human wildlife trader when it was being transported for sale in the market. “Maybe a young guy moves a pangolin and sold it on and may have had a mild infection but didn’t have any disease,” he said. “It’s not impossible for that scenario to happen.”
On the other hand, Hibberd believes it is possible the virus could have been brought back by one of the scientists, who were frequent travellers between the caves and Wuhan. “If you imagine these researchers who probably did this are students — who are probably quite young — it’s entirely possible that a researcher might become infected through the study of bats.”
The WIV was not the only body of scientists from the city delving into virus-laden caves. On December 10 last year a Chinese state media outlet published an extraordinary video lionising the bravery of a researcher called Tian Junhua, who is said to have caught 10,000 bats in studies for Wuhan’s disease control centre.
Tian admitted that he knew little about bats when he first started visiting the caves eight years ago, and once had to isolate himself for 14 days after being showered with bat urine while wearing inadequate protection. On occasions bat blood spilt onto his hands but he says he has never been infected.
The young researcher aroused suspicion because one of the offices of the disease control centre is about 300 yards from the Huanan seafood market. He has refused to talk to reporters, but his friends have firmly denied that he was “patient zero”.
The final and trickiest question for the WHO inspectors is whether the virus might have escaped from a laboratory in Wuhan. Is it possible, for example, that RaTG13 or a similar virus turned into Covid-19 and then leaked into the population after infecting one of the scientists at the Wuhan institute?
This seriously divides the experts. The Australian virologist Edward Holmes has estimated that RaTG13 would take up to 50 years to evolve the extra 4% that would make it a 100% match with the Covid-19 virus. Hibberd is slightly less conservative and believes it might take less than 20 years to morph naturally into the virus driving the current pandemic.
But others say such arguments are based on the assumption the virus develops at a constant rate, along lines that have been monitored over the past six months. “That is not a valid assumption,” said Ebright. “When a virus changes hosts and adapts to a new host the rate of evolutionary change is much higher. And so it is possible that RaTG13, particularly if it entered humans prior to November 2019, may have undergone adaptation in humans at a rate that would allow it to give rise to Sars-Cov-2. I think that is a distinct possibility.”
Ebright believes an even more controversial theory should not be ruled out. “It also, of course, is a distinct possibility that work done in the laboratory on RaTG13 may have resulted in artificial in-laboratory adaptation that erased those three to five decades of evolutionary distance.”
It is a view Hibberd does not believe is possible. “Sars-Cov-2 and RaTG13 are not the same virus and I don’t think you can easily manipulate one into the other. It seems exceptionally difficult,” he said.
Ebright alleges, however, that the type of work required to create Covid-19 from RaTG13 was “identical” to work the laboratory had done in the past. “The very same techniques, the very same experimental strategies using RaTG13 as the starting point, would yield a virus essentially identical to Sars-Cov-2.”
The Sunday Times put a series of questions to the WIV. They included why it had failed for months to acknowledge the closest match to the Covid-19 virus was found in a mine where people had died from a coronavirus-like illness. The questions were met with silence.
Commentary — although ultimately inconclusive, this is one of the most important — and best written — articles on the origins of the coronavirus pandemic that has appeared. Cudos to the Times of London for publising Revealed: Seven year coronavirus trail from mine deaths to a Wuhan lab!
The New York Times reports that the actual death rate of people infected by coronavirus is surprisingly low — “about 0.6 percent — which means that the risk of death is less than 1 percent.” Actually, the Times figures indicates that COVID-19 death rate is about 1/2 of 1 percent.
Stated another way, it now appears that less than one person out of every 100 who become infected with coronavirus may be expected to die. By comparison, the Bubonic plague is believed to have killed “an estimated 30–50 percent of the European population, between 1347–1351,” according to the U.S. National Library of Medicine National Institutes of Health. Thus the mortality rate from the Bubonic plague was as much as 100 times greater than the mortality rate from COVID-19.
Similarly, the mortality rate from the Spanish influenza was as much as 5 times greater than the mortality rate from COVID-19, and the Spanish influenza was simply a bad flu. According to the Center for Disease Control, the mortality rate from the 1919 Spanish influenza was about 2.5 percent, compared to about 1/2 of 1 percent for COVID-19.
Commentary — Despite hysterical and misleading headlines like “Covid-19 Deaths Soar in Florida…” in yesterday’s USA Today, the death rate from COVID-19 is actually quite low. And if the data from a recent Annals of Internal Medicine article reported in Science Daily is correct — that more than 90 percent of all COVID-19 infections are asymptomatic — then the actual COVID-19 death rate may be truly microscopic.
In fact, the novel coronavirus could be called a “minor league pandemic” because of the extremely low percentage of infected people it kills. The simple fact of the matter is that nearly everyone who contracts coronavirus survives.
Not everyone survives, of course, but better than 99 percent do in fact survive!
July 6, 2020 – Coronavirus death rate keeps dropping even as alarm grows over summer surge, Washington Times
The Washington Times reports that the number of Americans dying from COVID-19 has been falling for weeks, a case the White House is making as it points out that the U.S. fatality rate is well below that of Europe’s biggest countries.
White House press secretary Kayleigh McEnany told reporters Monday that the fatality rate — the ratio between confirmed deaths and confirmed cases — is well below that of France, the United Kingdom and Germany, as she defended President Trump’s comment during his Fourth of July address that 99% of novel coronavirus cases are “totally harmless.”
“The president is not downplaying the severity of the virus,” Ms. McEnany said at a press briefing. “What the president is noting is that at the height of this pandemic we were at 2,500 deaths per day. We are now at a place where on July 4 there were 254. That’s a tenfold decrease in mortality.”
She said the number of deaths from COVID-19 on Sunday was 209, which was down 23% from the previous week.
“What the president was pointing to, and I’m glad you brought it up, was a factual statement, one that is rooted in science and one that was pointing out the fact that mortality in the country is very low,” Ms. McEnany said.
Indeed, the Centers for Disease Control and Prevention issued an update Friday noting that the death rates from pneumonia, influenza and COVID-19 have dropped for 10 straight weeks, from 9.0% in week 25 to 5.9% in week 26 and almost reaching the point at which the outbreak would no longer be considered an epidemic.
“The percentage is currently at the epidemic threshold but will likely change as more death certificates are processed, particularly for recent weeks,” the CDC said in its July 3 update.
After daily death rates peaked at 3,000 in March and April, they fell Sunday to 251, in large part because younger people who are better able to survive COVID-19 make up a larger percentage of patients.
Alex Berenson, author of “Unreported Truths About Covid-19 and Lockdowns,” said the “news is significantly better on all fronts” when it comes to SARS-CoV-2, the official name of the virus.
“Despite fact that the number of positive SARS-COV-2 tests (what the media calls cases) in the Sun Belt has been rising for the last few weeks, hospitalizations and especially patients in intensive care and on ventilators are rising much more slowly,” Mr. Berenson said.
In addition, “deaths actually continue to drop to their lowest levels since the epidemic began in March.”
Mr. Trump said in a Twitter post that COVID-19 deaths in the U.S. have fallen by more than a third and asked why the “Lamestream Fake News Media REFUSE to say that China Virus deaths are down 39%, and that we now have the lowest Fatality (Mortality) Rate in the World.
“They just can’t stand that we are doing so well for our Country!” the president tweeted.
MedPage Today writes that Broadway star Nick Cordero has lost his over-three-month battle with COVID-19 at the age of 41. Cordero’s Broadway credits include “Waitress,” “Rock of Ages,” “A Bronx Tale,” and “Bullets Over Broadway.”
Many have been following the roller coaster ride that has been Cordero’s medical course through the frequent Instagram posts of his wife Amanda Kloots. A previously healthy Cordero fell ill on March 20, with an initial diagnosis of pneumonia. After two negative tests, a third was positive for COVID-19. He was admitted from the emergency department on March 30 and was intubated on a ventilator on April 1.
“Since then has [sic] he has suffered an infection that caused his heart to stop, he needed resuscitation, he had two mini strokes, went on ECMO, went on dialysis, needed surgery to remove an ECMO cannula that was restricting blood flow to his leg, a fasciotomy to relieve pressure on the leg, an amputation of his right leg, an MRI to further investigate brain damage, several bronchial sweeps to clear out his lungs, a septic infection causing septic shock, a fungus in his lungs, holes in his lungs, a tracheostomy, blood clots, low blood count and platelet levels, and a temporary pacemaker to assist his heart.”
On May 1, he was taken off sedation but did not regain consciousness until May 13. Although he was able to respond slightly with his eyes, he remained immobile. His lung damage was so severe that Kloots told CBS This Morning that it was likely that Nick would need a double lung transplant, “in order to live the kind of life that I know my husband would want to live.”
Commentary — The supposedly “humanitarian” effort to save people who are very sick with COVID-199 is frequently not an act of kindness, as the case of Broadway star Nick Cordero shows. The true kindness is to let them die, for as the country song says, “the secret to a long life is knowing when it’s time to go.”
July 9, 2020 – 68% of a New York clinic’s patients test positive for coronavirus antibodies, New York Times (Commentary)
The New York Times reports that people living in some of the areas of New York City hit hardest by COVID-19 also have the highest incidence of COVID-19 resisting antibodies.
The data, first reported by The New York Times Thursday, shows that more than 68% of people tested positive for antibodies at a clinic in Corona, Queens, while 56% tested positive at another clinic in Jackson Heights, Queens.
While these two working-class neighborhoods saw high numbers for their antibody tests, only 13% of people tested positive for antibodies at a clinic in Cobble Hill, a mostly white and wealthy neighborhood in Brooklyn. The data suggest that while minority and working-class communities were hit hard by the virus, they may be first to build immunity.
“When you’re looking at a large population of people and a large percentage of those people are technically immune to a virus, you could start thinking it’ll be almost impossible for the virus to penetrate and for people to get sick,” said Dr. Daniel Frogel, senior vice president of medical operations at CityMD.
Commentary — This data suggests that attempting to limit COVID-19 exposure and infections may be completely wrong-headed and counter-productive. To achieve herd immunity, a high rate of coronavirus infection may necessary.
In other words, it may be that face masks should be prohibited, not made mandatory.
And the most exciting thing about this New York study is that the COVID-19 antibody rates of 60 percent or better seen in hard hit New York neighborhoods would appear to be enough to grant the population herd immunity!
In fact, if two recent articles in Atlantic Monthly and The Conversation / Umeå University are correct, 60 percent coronavirus antibodes may be THREE TIMES more than are needed to achieve herd immunity against the coronavirus pandemic.
Health reports that in the very small minority of COVID-19 infections where the individuals show symptoms from the infection, the damage wrought by the virus can be widespread and severe.
Coronavirus can damage not only the lungs, but the kidneys, liver, heart, brain and nervous system, skin and gastrointestinal tract, according to doctors from Columbia University Irving Medical Center in New York City.
Their comprehensive picture shows the coronavirus attacks virtually every major system in the human body, directly damaging organs and causing the blood to clot, the heart to lose its healthy rhythm, the kidneys to shed blood and protein and the skin to erupt in rashes. It causes headaches, dizziness, muscle aches, stomach pain and other symptoms along with classic respiratory symptoms like coughing and fever.
Much of the damage wrought by the virus appears to come because of its affinity for a receptor — a kind of molecular doorway into cells — called ACE2. Cells lining the blood vessels, in the kidneys, the liver ducts, the pancreas, in the intestinal tract and lining the respiratory tract all are covered with ACE2 receptors, which the virus can use to grapple and infect cells, the Columbia team wrote in their review, published in the journal, Nature Medicine.
Blood clotting effects appear to be caused by several different mechanisms: direct damage of the cells lining the blood vessels and interference with the various clotting mechanisms in the blood itself. Low blood oxygen caused by pneumonia can make the blood more likely to clot, the researchers said.
These clots can cause strokes and heart attacks or can lodge in the lungs or legs. They clog the kidneys and interfere with dialysis treatments needed for the sickest patients.
Damage to the pancreas can worsen diabetes, and patients with diabetes have been shown to be at the highest risk of severe illness and death from coronavirus.
The virus can directly damage the brain, but some of the neurological effects likely come from the treatment.
“COVID-19 patients can be intubated for two to three weeks; a quarter require ventilators for 30 or more days,” according to the study. “These are very prolonged intubations, and patients need a lot of sedation. ‘ICU delirium’ was a well-known condition before COVID, and the hallucinations may be less an effect of the virus and more an effect of the prolonged sedation.”
The virus also affects the immune system, depleting the T-cells the body usually deploys to fight off viral infections. “Lymphopenia, a marker of impaired cellular immunity, is a cardinal laboratory finding reported in 67-90% of patients with [symptomatic] COVID-19” infections, the researchers wrote.
Commentary — As many as 96 percent of people infected with the coronavirus are asymptomatic and don’t even know they are infected, but a small minority of those infected may suffer a wide range of harmful bodily effects, including damage to the lungs, heart, kidneys, pancreas, immune system and brain.
However, some of this damage — such as dementia — may be the result of ill-advised hospital “treatments,” such as prolonged intubation on ventilators.
July 10, 2020 – Covid-19 Immunity May Rely on a Microscopic Helper: T Cells, Wired (Commentary)
Wired reports that researchers have been looking beyond antibodies to understand how immunity to the new virus might work—and how to design a vaccine.
If you want to know if you’ve ever been infected with SARS-CoV-2 (COVID-19), the natural thing to do is to get a blood test. These look for antibodies—proteins that signal your body has encountered a virus, and could perhaps be protected from catching it again. But recently, a study published in Nature Medicine introduced a worrying complication. Researchers in Chongqing, China, followed 37 people who had tested positive for the virus but didn’t show symptoms during their illness—in other words, who were asymptomatic—and tested their blood regularly. They found those antibodies didn’t always last for long: In some cases, after two to three months, they were barely detectable. Thought a positive antibody test was your ticket out of this thing? It’s not so simple. Simple, after all, is not a word immunologists would ever use to describe their field.
Marcus Buggert, an immunologist at the Karolinska Institute in Sweden, had noticed a similar pattern among patients there: cases where people who tested positive for the virus quickly lost their antibodies or never appeared to muster those forces at all. That wasn’t a big surprise—antibodies had also waned in patients who recovered from SARS. But to Buggert, who studies T cells—part of an orchestra of cells that perform in the body’s immune response—the symphony appeared incomplete. Research from SARS offered hints that, even if antibodies faded, some people retained immune cells that recognized the virus. Sometimes, those responses could last for years. For SARS-CoV-2, similar dimensions of the immune response could have bearing on how immunity works and how to design a vaccine. “Just because you can’t detect antibodies in their blood doesn’t mean there’s no immune response,” Buggert says.
Antibodies are a critical component of immunity—especially the ones that “neutralize” the virus by homing in on the proteins that comprise it. They glom onto their target and prevent the virus from infecting cells. A good vaccine will try to replicate that kind of natural protection. “Neutralizing antibodies are the holy grail,” says Sallie Permar, a vaccine researcher at Duke University. “There are few to no viral vaccines where we’re not shooting for that as an end point.”
But antibody levels are only part of the immunity story. While antibodies may wane past the limit of detection, that doesn’t mean they go away entirely. And even a very low level could be protective. “What‘s important when you’ve been exposed to the virus is how quickly you can ramp up those antibodies,” Permar says. That involves a whole army of cells, which store knowledge of each new pathogen they encounter. There are B cells, which help coax those virus-specific antibodies into existence, plus killer T cells, which can learn to obliterate infected cells. Helper T cells help orchestrate the whole process. “You have multiple arms of the immune response,” says Donna Farber, an immunologist at Columbia University who studies respiratory viruses. “It’s like the Army, the Navy, and the Air Force.” If one branch stands down, the body hasn’t necessarily lost its germ-fighting capacity.
For vaccine researchers, those helper T cells are of particular interest. They’re the ones that rally the troops, kicking off the process that leads to antibody production. But so far, there hasn’t been evidence that that’s how the body is actually primed to fight SARS-CoV-2, says John Wherry, an immunologist at the University of Pennsylvania. That’s because T cell responses are much harder to measure than antibody levels, requiring a lot of blood and fine-tuned instrumentation to wrangle the right kinds of immune cells. “We’ve lacked data on which cells—especially B and T cells—are truly recognizing the virus,” Wherry says. “There’s a lot of noise.”
That makes it difficult to know if vaccine developers are really on the right track. Their hunch is based, primarily, on how the immune system responds to other pathogens. But some viruses evade the typical patterns. They short-circuit the immune response. The most infamous example of that is HIV, Wherry says, which attacks the very T cells that would coordinate the immune response to the virus. SARS-CoV-2 has already offered its own twists and turns, like its propensity to prompt runaway immune responses. For Covid-19, “there’s no prototypical immune response, especially in severe cases,” Wherry says.
Lately, though, systematic studies of T and B cell responses to SARS-CoV-2 have begun to elicit some patterns. Recently, researchers at the La Jolla Institute for Immunology looked at T cell responses in what they considered “average” cases of the disease—people who got sick but didn’t need to be hospitalized. In a study published in Cell in May, they found that all of their subjects developed helper T cells, and 70 percent had killer T cells. The level of the T cell response, they found, roughly corresponded with levels of neutralizing antibodies. Other studies, including a recent preprint from a team at Oxford, have come to similar conclusions.
Simply having T cells—or even antibodies—that recognize the virus doesn’t mean you’re protected. There’s much more to learn about that. But on the vaccine front, the findings looked like good news. “It’s confirming that [helper] T cells are going to be an important factor in generating a robust antibody response,” Permar says. That’s a relief for pharma companies trying to replicate that process with a vaccine.
But immunology is never straightforward, remember? The La Jolla group’s findings came with a wrinkle: In a control group of blood donors who had never been exposed to SARS-CoV-2, the researchers also found T cells that recognized the virus. They speculate that those T cells might be “cross-reactive” with other viruses. Say you’ve had a lot of colds—especially colds caused by other coronaviruses. Then perhaps your immune system is primed to recognize this new virus based on its experience with other viral proteins, the researchers suggested.
It’s too soon to tell if those particular T cells offer any useful protection against SARS-CoV-2, the researchers caution. (In fact, let’s just make that the blanket caveat, for now.) But cross-reactive cells could have implications for vaccines too, Permar says. Those T cells could be a good thing, if they give their bearers a head start in producing antibodies after vaccination. Or they could backfire if a vaccine stimulates them to generate the wrong kind of antibodies, elbowing out a more fine-tuned response to SARS-CoV-2.
And what about when those antibodies wane in exposed people, or if they don’t show up at all? To address that question, Buggert’s team in Sweden took a slightly different approach. In addition to Covid-19 patients and two control groups—blood donors who gave samples before and after the pandemic began—they added members from the households of people with known cases. Those people, they reasoned, were at a greater likelihood of having been exposed to the virus than the general population, even if they had never shown symptoms or got tested.
Like other researchers, Buggert’s team saw cross-reactive T cells in unexposed people. But they also looked for responses that were specific to this virus by identifying a unique array of viral proteins those T cells recognized—a response not seen in the pre-pandemic blood donors. “People who have really been infected [with SARS-CoV-2] tend to respond against multiple different regions of the virus,” Buggert explains. “They have a broader response.” In a few blood donations taken during the pandemic, and in the household members of Covid-19 patients, they found that unique T cell response, but no antibodies.
That research hasn’t been peer-reviewed yet. And it’s a small study, Farber notes, with plenty of uncertainty; ruling out cross-reactivity entirely is a difficult task. “I think you need really big cohort studies to assess that this is possible,” she says. And in any case, back to that original caveat: Nothing about the results says that a T cell response alone confers immunity to Covid-19. But to Buggert, it demonstrates the importance of looking beyond antibodies alone when investigating potential immunity.
Commentary — This is an interesting and thoughtful piece that takes the herd immunity discussion in America beyond the hysterical, dumb-think coverage seen in sources like CNN (“We’re wasting our time talking about herd immunity”).
Here’s an absolute, unequivocal fact of the matter — herd immunity is what has gotten the human species through every pandemic we have ever faced, and it is what will get us through this one. The only question here is really how many people will have to die to achieve herd immunity protection.
With a vaccine, herd immunity can be achieved without great loss of human life. Without a vaccine, it will take mass graves. But either way, herd immunity is humanity’s ONLY way out of the COVID-19 pandemic.
Dr. Li-Meng Yan told Fox News that she believes China knew about the coronavirus well before it claimed it did. She says her supervisors also ignored research she was doing that she believes could have saved lives.
Yan’s story weaves an extraordinary claim about cover-ups at the highest levels of government and seemingly exposes the obsessive compulsion of President Xi Jinping and his Communist Party to control the coronavirus narrative: what China knew, when it knew it and what edited information it peddled to the rest of the world.
Yan said a scientist at the Center for Disease Control and Prevention in China who had first-hand knowledge of the cases told her on Dec. 31, 2019 about human-to-human transmission well before China or the WHO admitted such spread was possible.
She reported some of these early findings back to her boss, Yan said.
“He just nodded,” she recalled, and told her to keep working.
A few days later, on Jan. 9, 2020, the WHO put out a statement: “According to Chinese authorities, the virus in question can cause severe illness in some patients and does not transmit readily between people… There is limited information to determine the overall risk of this reported cluster.”
She also claims the co-director of a WHO-affiliated lab, Professor Malik Peiris, knew but didn’t do anything about it.
The WHO and China have vehemently denied claims of a coronavirus cover-up.
July 11, 2020 – 80% Of People Hospitalized With Coronavirus Still Had Symptoms Two Months Later, Says New Study, Forbes (Commentary)
Forbes reports that a new study looking at people discharged from hospital after treatment for COVID-19 has found that 80 percent of them were still reporting symptoms two months later.
The research published in the Journal of the American Medical Association looked at 143 patients from Italy who had been hospitalized with Covid-19 and survived.
At the time of the assessment, none of the patients reported fever, or any symptoms of acute COVID-19 but over half reported fatigue and 43% reported shortness of breath. Almost a third of the survivors reported joint pain and 22% had chest pain.
Only 13% of patients were free of any COVID-19-related symptoms after two months, whereas more than 50 percent of the people reported three or more symptoms. People profiled in this study were between 19-84 years old, with an average age of 57.
In some people, COVID-19 can cause persistent and long-lasting symptoms, even long after the virus itself can no longer be detected.
Commentary — while COVID-19 does not make most people sick, and more than 99 percent of those infected survive, it does cause serious, persistent health issues for a small minority of those people who become infected with the disease.
July 12, 2020 – Florida’s 15,300 new COVID-19 cases sets a new U.S. pandemic record, South Florida Sun-Sentinel (Commentary)
The South Florida Sun-Sentinel reports that Florida hit an alarming one-day high on Sunday with 15,300 new coronavirus cases, shattering both the state and national record for new cases reported since the start of the pandemic.
With Sunday’s staggering surge in new cases, Florida eclipsed New York’s coronavirus peak of 12,274 cases on April 4.
Researchers say they expect deaths to rise nationwide in the coming weeks, but some aren’t expecting the numbers to spike as dramatically as they did in the spring partly due to increased testing.
Adm. Brett Giroir, a member of the White House coronavirus task force, says mask-wearing is key to curbing the spread of the potentially fatal virus.
“If we don’t have that, we will not get control of the virus,” Giroir, assistant secretary at the Health and Human Services Department, told ABC’s “This Week” on Sunday.
Florida reported 45 new deaths Sunday morning. That’s a lower tally than in the past several days.
On Thursday, Florida reported 120 deaths in one day, setting a state record for daily deaths during the pandemic. On Saturday, two days later, Florida tallied its second-most deaths in a day, with 98. Friday’s death toll was also high, at 93.
Commentary — Despite the heavy breathing note of terror in this story, it is actually very good news that Florida is experiencing record numbers of new coronavirus cases!
We as a nation and a species need as many people as possible to get the coronavirus so that the “herd” can achieve immunity.
As a recent article in the Atlantic notes, places like New York City that were hammered by the first wave of the coronavirus pandemic “have now achieved “a version of herd immunity, or at least safe equilibrium,” with low numbers of new infections, BECAUSE THEY WERE HAMMERED.
In fact, recent studies show that the hardest hit New York neighborhoods have coronavirus antibodies in as high as 60 percent of the population, while less hard hit neighborhoods only have antibodies in less than 20 percent of the population.
Herd immunity is what has gotten the human species through every pandemic we have ever faced, and it is what will get us through this one. The only question here is really how many people will have to die to achieve herd immunity protection.
With a vaccine, herd immunity can be achieved without great loss of human life. Without a vaccine, it will take mass graves. But either way, herd immunity is humanity’s ONLY way out of the COVID-19 pandemic.
But you can’t ride on the herd immunity bus unless you pay the fare, and the cost here is that many people must get infected (the majority of whom will be asymptomatic and not even know they are sick) , and a few (about 1/2 of 1 percent of those infected) must die so the majority may live.
Them’s the hard facts of the matter. We’re not dealing with a stroll in the park here; we’re dealing with a pandemic!
July 12, 2020 – Russia first nation to finish human trials of Coronavirus vaccine, Tass News Agency
Russian news agency TASS reports that Russia has become the first country to complete human trials of the COVID-19 vaccine on Sunday, July 12. The Russian news agency added that the results have proven the effectiveness of the medication.
Human trials have been completed at the Sechenov University, and the subjects of the study will soon be discharged, said chief researcher Elena Smolyarchuk who heads the Center for Clinical Research on Medications at the university.
“The research has been completed and it proved that the vaccine is safe. The volunteers will be discharged on July 15 and July 20,” said Smolyarchuk in an interview with TASS.
However, there was no further information yet on when their vaccine would be commercially reproduced. On June 18, Russia had allowed clinical trials of two forms of a potential COVID-19 vaccine developed by the Gamaleya National Research Center for Epidemiology and Microbiology.
Moreover, Burdenko Military Hospital received the first vaccine in the form of a solution for intramuscular administration. Then another vaccine in the form of a powder for preparing the solution for an intramuscular administration was carried out at the Sechenov First Moscow State Medical University.
The first stage of the Sechenov University vaccine research involved 18 volunteers in one group and a second group with 20 volunteers. After the vaccination, the volunteers were expected to remain isolated in a hospital for 28 days.
Early results of the vaccine tests on a group of volunteers showed that they were developing antibodies to the coronavirus.
July 12, 2020 – Coronavirus: Could It Be Burning Out After 20 Percent of a Population Is Infected?, The Conversation (Commentary)
More than half a million people have died from COVID-19 globally. It is a major tragedy, but perhaps not on the scale some initially feared. And there are finally signs that the pandemic is shuddering in places as if its engine is running out of fuel.
On the Diamond Princess cruise ship, for example, where the virus is likely to have spread relatively freely through the air-conditioning system linking cabins, only 20 percent of passengers and crew were infected. Data from military ships and cities such as Stockholm, New York, and London also suggest that infections have been around 20 percent – much lower than earlier mathematical models suggested.
This has led to speculation about whether a population can achieve some sort of immunity to the virus with as little as 20 percent infected – a proportion well below the widely accepted herd immunity threshold (60-70 percent).
The Swedish public health authority announced in late April that the capital city, Stockholm, was “showing signs of herd immunity” – estimating that about half its population had been infected. The authority had to backtrack two weeks later, however, when the results of their own antibody study revealed just 7.3 percent had been infected. But the number of deaths and infections in Stockholm is falling rather than increasing – despite the fact that Sweden hasn’t enforced a lockdown.
Hopes that the COVID-19 pandemic may end sooner than initially feared have been fuelled by speculation about “immunological dark matter”, a type of pre-existing immunity that can’t be detected with coronavirus antibody tests.
Antibodies are produced by the body’s B-cells in response to a specific virus. Dark matter, however, involves a feature of the innate immune system termed “T-cell mediated immunity”. T-cells are produced by the thymus and when they encounter the molecules that combat viruses, known as antigens, they become programmed to fight the same or similar viruses in the future.
Studies show that people infected with COVID-19 indeed have T-cells that are programmed to fight this virus. Surprisingly, people never infected also harbor protective T-cells, probably because they have been exposed to other coronaviruses. This may lead to some level of protection against the virus – potentially explaining why some outbreaks seem to burn out well below the anticipated herd immunity threshold.
Young people and those with mild infections are more likely to have a T-cell response than old people – we know that the reservoir of programmable T-cells declines with age.
In older and immunocompromised populations like the Italian COVID-19 epicenter in Bergamo, a town where one in four residents are pensioners, 60 percent of the population had antibodies by early June.
Commentary — this article offers a glimmer of real hope that herd immunity may be achieved against the coronavirus pandemic without the introduction of an effective vaccine, which may never actually happen. It also echoes the recent story in Atlantic Monthly which suggests that if 20 percent of the population has coronavirus antibodies, it may be enough to achieve herd immunity.
The Atlantic Monthly writes that the herd immunity threshold in the United States might be achieved with “less than 20 percent” of the population infected by COVID-19 and therefore possessing coronavirus antibodies, compared to the 65 percent that many scientists have though would be required to obtain herd immunity.
Here’s why — there is enormous variation even within the U.S. in terms of the impact of the coronavirus pandemic. Some places took limited measures and were barely hit; others locked down but suffered greatly. New York City has been slowly reopening since early June, but despite that—and despite mass outdoor gatherings in the throes of civil unrest over the past six weeks—the city has not seen even a small increase in daily reported cases. By contrast, other cities that have attempted to reopen have seen incapacitating surges.
In a pandemic, the differences the infectious process for different locales and different groups of people make forecasting difficult. When you flip a coin, the outcome is not affected by the flips prior. But in dynamic systems, the outcomes are more like those in chess: The next play is influenced by the previous one. Differences in outcome can grow exponentially, reinforcing one another until the situation becomes, through a series of individually predictable moves, radically different from other possible scenarios. You have some chance of being able to predict the first move in a game of chess, but good luck predicting the last.
That’s exactly what Gabriella Gomes, a professor at the University of Strathclyde, in Glasgow, Scotland, attempts to do. She describes a model in which everyone is equally susceptible to coronavirus infection (a homogeneous model), and a model in which some people are more susceptible than others (a heterogeneous model). Even if the two populations start out with the same average susceptibility to infection, you don’t get the same epidemics. “The outbreaks look similar at the beginning. But in the heterogeneous population, individuals are not infected at random,” she told me. “The highly susceptible people are more likely to get infected first. As a result, the average susceptibility gets lower and lower over time.”
Effects like this—“selective depletion” of people who are more susceptible—can quickly decelerate a virus’s spread. When Gomes uses this sort of pattern to model the coronavirus’s spread, the compounding effects of heterogeneity seem to show that the onslaught of cases and deaths seen in initial spikes around the world are unlikely to happen a second time. Based on data from several countries in Europe, she said, her results show a herd-immunity threshold much lower than that of other models.
“We just keep running the models, and it keeps coming back at less than 20 percent” to achieve herd immunity, Gomes said. “It’s very striking.”
If that proves correct, it would be life-altering news. It wouldn’t mean that the virus is gone. But by Gomes’s estimates, if roughly one out of every five people in a given population is immune to the virus, that seems to be enough to slow its spread to a level where each infectious person is infecting an average of less than one other person. The number of infections would steadily decline. That’s the classic definition of herd immunity. It would mean, for instance, that at 25 percent antibody prevalence, New York City could continue its careful reopening without fear of another major surge in cases.
At Stockholm University, Tom Britton, the dean of mathematics and physics, thinks that a 20 percent threshold is unlikely, but not impossible. His lab has also been building epidemiological models based on data from around the globe. He believes that variation in susceptibility and exposure to the virus clearly seems to be reducing estimates for herd immunity. Britton and his colleagues recently published their model, demonstrating the effect, in Science.
“If there is a large variability of susceptibility among humans, then herd immunity could be as low as 20 percent,” Britton told me. But there’s reason to suspect that people do not have such dramatically disparate susceptibility to the coronavirus. High degrees of variability are more common in things such as sexually transmitted infections, where a person with 100 partners a year is far more susceptible than someone celibate. Respiratory viruses tend to be more equal-opportunity invaders. “I don’t think it will happen at 20 percent,” Britton said. “Between 35 and 45 percent—I think that would be a level where spreading drops drastically.”
“During the last few months, we’ve started talking about ‘natural herd immunity’ and what would be used to block future waves,” says Shweta Bansal, an associate professor at Georgetown University who studies how social interactions influence infectious diseases. She worries that many people conflate academic projections about reaching herd immunity with a “let it run wild” fatalism. “My view is that trying to take that route would lead to mass death and devastation,” she says.
But some areas have had no choice but to let the virus “run wild,” and they are now experiencing the benefits. Essentially, at present, New York City — which was hit very hard by the first coronavirus wave — might be said to be at a version of herd immunity, or at least safe equilibrium. Our case counts are very low. They have been low for weeks. Our antibody counts mean that a not-insignificant number of people are effectively removed from the chain of transmission. Many more can be effectively excluded because they’re staying isolated and distanced, wearing masks, and being hygienically vigilant. If we keep living just as we are, another big wave of disease seems unlikely.
Commentary — This is a rambling and hard to understand story that is nonetheless important, partly for what it says and partly for what it doesn’t want to say for fear of being “politically incorrect.”
The point of the story is that it may be possible to achieve herd immunity against the coronavirus pandemic with only 20 percent immunity in the broad population, or less than one third the percentage many scientists have thought up until now. This is very good news!
The second, implicit point of the story is that places like New York City, which was hammered by the first wave of the coronavirus pandemic, have now achieved “a version of herd immunity, or at least safe equilibrium,” with low numbers of new infections, BECAUSE THEY WERE HAMMERED.
In fact, recent studies show that the hardest hit New York neighborhoods have coronavirus antibodies in as high as 60 percent of the population, while less hard hit neighborhoods only have antibodies in less than 20 percent of the population.
You can’t ride on the herd immunity bus unless you pay the fare, and the cost here is that many people must get infected (the majority of whom will be asymptomatic and not even know they are sick) , and a few (about 1/2 of 1 percent of those infected) must die, or experience what the story euphemistically calls “selective depletion.” Them’s the hard facts of the matter. We’re not dealing with a stroll in the park here; we’re dealing with a pandemic!
July 13, 2020 – Coronavirus warning from Italy: Effects of COVID-19 could be worse than first thought, Sky News (Commentary)
According to Sky News, the long-term effects of COVID-19, even on people who suffered a mild infection, could be far worse than was originally anticipated, according to researchers and doctors in northern Italy.
Psychosis, insomnia, kidney disease, spinal infections, strokes, chronic tiredness and mobility issues are being identified in former coronavirus patients in Lombardy, the worst-affected region in the country.
The doctors warn that some victims may never recover from the illness and that all age groups are vulnerable.
The virus is a systemic infection that affects all the organs of the body, not, as was previously thought, just a respiratory disease, they say.
Some people may find that their ability to properly work, to concentrate, and even to take part in physical activities will be severely impaired.
“At first, initially, we thought it was a bad flu, then we thought it was a bad flu with a very bad pneumonia, but subsequently we discovered that it is a systemic illness with vessel damage in the whole body with renal involvement, cerebral involvement,” Dr. Roberto Cosentini, head of emergencies at Papa Giovanni XXIII Hospital in Bergamo, Italy, said.
Italian researchers identified serious neurological complications arising from COVID-19 including delirium, brain inflammation, stroke and nerve damage in 43 people aged 16 to 85.
Some of the patients had experienced no severe breathing problems at all, with the neurological disorder being the first and only sign that they had coronavirus.
Commentary — The supposedly “humanitarian” effort to save people who are very sick with COVID-199 is frequently not an act of kindness, as the case of Broadway star Nick Cordero shows. The true kindness is to let them die, for as the country song says, “the secret to a long life is knowing when it’s time to go.”
But as the New York Times has calculated, more 99 percent of the people who become infected with the coronavirus do NOT die. They survive, and the majority do not even know they were “sick.”
And to beat the coronavirus, this is exactly what must happen. We need as many people as possible to get sick and survive. As a recent article in the Atlantic notes, places like New York City that were hammered by the first wave of the coronavirus pandemic “have now achieved “a version of herd immunity, or at least safe equilibrium,” with low numbers of new infections, BECAUSE THEY WERE HAMMERED.
And this is also true of the Italian town that is the scene of this story. Bergamo, Italy, has an elderly population, and was especially hard hit by the first wave of the coronavirum pandemic. However, tests show that more than 60 percent of Bergamo’s population now has coronavirus antibodies which impart at least some immunity to the disease.
A reflection of this is the fact that Dr. Roberto Cosentini was interviewed for this story in a silent hospital emergency room, a stark contrast to the busy emergency room scene at Papa Giovanni XXIII Hospital a few months ago.
CNBC writes that U.S. health officials and drugmakers expect to start producing potential coronavirus vaccine doses by the end of the summer, a senior administration official said Monday.
The U.S. is aiming to deliver 300 million doses of a vaccine for Covid-19 by early 2021. The manufacturing process is already underway even though they aren’t sure which vaccine, if any, will work, a senior Trump administration official told reporters on a conference call Monday. He said they are already buying equipment, securing the manufacturing sites and, in some cases, acquiring the raw materials.
“Exactly when the vaccine materials will be in production and manufacturing? It’s probably four to six weeks away,” the official said on the call, which was hosted by the Department of Health and Human Services. “But we will be actively manufacturing by the end of the summer.”
Because of the pandemic, U.S. health officials and researchers have been accelerating the development of vaccine candidates by investing in multiple stages of research even though doing so could be for naught if the vaccine ends up not being effective or safe.
U.S. health officials have previously said they are ramping up the manufacturing process to ensure they can immediately get a vaccine to market once they identify one that works.
The Trump administration has selected four potential vaccines as the most likely candidates, but the senior official said Monday that that list could grow. On the list are vaccines from biotech firm Moderna and Johnson & Johnson. The two companies are expected to begin late-stage human trials for potential vaccines by the end of this month. It’s a record-breaking time frameto produce a vaccine — even as scientists say there is no guarantee the vaccines will be effective.
President Donald Trump has repeatedly touted the “tremendous progress” of vaccine development, calling the project Operation Warp Speed, as coronavirus cases across the U.S. continue to surge.
July 13, 2020 – Why a coronavirus vaccine won’t end the pandemic by itself, San Francisco Chronicle
The San Francisco Chronicle writes that a vaccine may not be enough to end the coronavirus pandemic and restore society to some semblance of normalcy, according to doctors and researchers who say effective treatments for COVID-19 are equally important.
While many parts of public life, from crowded stadiums to San Francisco’s beloved cable cars, are on hold until the threat posed by the virus abates, a vaccine alone will likely not allow those functions to resume. And even if scientists find a vaccine that works and is safe, it may take a long time to reach everyone who needs it.
In the meantime, millions of people will continue to become ill with the coronavirus. So researchers across the globe are racing to find drugs that can keep more people alive and out of the hospital — and any one of those treatments may ultimately work just as well as a vaccine.
“I’d much rather put my money on the drugs rather than the vaccine for now,” said Dr. Lee Riley, an infectious-disease expert at UC Berkeley’s School of Public Health.
A drug could function similarly to a vaccine if it can prevent people from transmitting the virus in addition to improving their symptoms, Riley said. For example, people can protect themselves from being infected with HIV by regularly taking a pre-exposure prophylaxis, or PrEP, a pill sold under the brand-name Truvada and made by Foster City’s Gilead Sciences.
To accomplish something similar for the coronavirus, drug makers would need to develop a pill that people could take as soon as they begin having symptoms or even as a preventative measure akin to Truvada, Riley said. If a drug along those lines works to prevent people from falling ill with COVID-19, people can start going back to work and school much more easily, he said.
So far, the highest-profile and most advanced drug used to treat COVID-19 is remdesivir, an antiviral medicine that is also made by Gilead. Clinical trials have shown that hospitalized patients who received the drug through intravenous injections recovered faster than those who did not get the treatment, and Gilead revealed data on Friday indicating that remdesivir can help people survive, too. In a recent study of hundreds of coronavirus patients, remdesivir reduced mortality risk by 62%, the company said.
Gilead now is studying an inhalable form of remdesivir. If proved safe, the inhalable version of the drug could be given to patients who are not hospitalized, potentially slowing the spread of the virus.
July 13, 2020 – WHO: We won’t immediately have a ‘perfect vaccine’, Business Insider
Business Insider writes that a coronavirus vaccine is still many months away, but leading infectious disease experts are already warning that any eventual inoculation won’t be a one-and-done fix for this pandemic, and that we’ll instead have to learn to live with the looming threat of more coronavirus infections for months, if not years to come.
“Expecting that we will eradicate or eliminate this virus in the coming months is not realistic,” the World Health Organization’s Mike Ryan, executive director of health emergencies, said during a press briefing streamed from Geneva on Monday.
“And also, believing that magically we will get a perfect vaccine that everyone will have access to, is also not realistic.”
Ryan’s notes of caution about eradicating the novel coronavirus, and the disease it causes — COVID-19 — come as the respiratory virus continues rapidly circling the globe, while infecting tens of thousands of new people across the US every day. On Sunday, Florida reported more than 15,000 new COVID-19 cases in a single day, a new record for any US state.
July 13, 2020 – CDC Director Pleads for Mask Compliance: If Everybody Wears One for Six Weeks, We Could Drive Covid ‘Into the Ground’, Mediate.com (Commentary)
Mediaite.com reports that CDC Director Robert Redfield pleaded with people to wear masks in a press conference Monday afternoon, declaring that Americans could drive Covid-19 “into the ground” if everybody wore facial coverings for six weeks.
“If everyone could wear a face covering over the next six weeks we could drive this [coronavirus] into the ground,” Redfield said in Mecklenburg County, NC. Mecklenburg County, which includes Charlotte, has more than seven times the number of Covid-19 positive cases than any other county the state.
Redfield’s comments come as the United States has seen three-straight days of 60,000-plus new coronavirus cases.
The CDC recommends but does not require “people wear cloth face coverings in public settings and when around people who don’t live in your household, especially when other social distancing measures are difficult to maintain,” according to its website.
Commentary — if that’s all it takes, count me in!
July 14, 2020 – World’s first recorded case of a child contracting COVID-19 from its mother inside the womb, Business Insider
Business Insider reports that Doctors in France have reported what they say is the first confirmed case of a child contracting the coronavirus from their mother while still in the womb.
The case was the subject of a paper titled “Transplacental transmission of SARS-CoV-2 infection,” published Tuesday in the peer-reviewed journal Nature Communications. Details of the paper were first reported by The Guardian.
Until now, there has been limited evidence suggesting that a child could catch the coronavirus from inside the womb, but the paper’s authors, from the Antoine Béclère hospital, in Paris, confirmed “transplacental transmission of SARS-CoV-2” was possible.
They said a 23-year-old woman was admitted to the hospital with a fever and cough on March 24 when she was more than 35 weeks pregnant with a boy.
The mother tested positive for the coronavirus, gave birth by cesarean section, and the baby was immediately taken to the natal intensive care unit.
The baby tested positive for the virus. He later recovered and was discharged 18 days later, the doctors said.
They said the baby’s brain bore evidence of inflammation caused by the coronavirus, which had crossed the placenta into the baby’s bloodstream.
They ruled out the chance that the baby caught the virus after birth by viral or bacterial means.
“The placenta showed signs of acute and chronic intervillous inflammation consistent with the severe systemic maternal inflammatory status triggered by SARS-CoV-2 infection,” the authors said.
July 14, 2020 – A Look at the Coronavirus Reinfection Rate, National Review
National Review reported that yesterday brought two stories that seemed like just about the worst news we could get in this pandemic. First, the Guardian over in the U.K. reported on a study by King’s College London suggesting that after infection, coronavirus patients could lose their built-in immunity to reinfection fairly quickly:
Blood tests revealed that while 60 percent of people marshalled a “potent” antibody response at the height of their battle with the virus, only 17 percent retained the same potency three months later. Antibody levels fell as much as 23-fold over the period. In some cases, they became undetectable.
“People are producing a reasonable antibody response to the virus, but it’s waning over a short period of time and depending on how high your peak is, that determines how long the antibodies are staying around,” said Dr Katie Doores, lead author on the study at King’s College London.
Then, over in Vox, D. Clay Ackerly, an internal medicine and primary-care physician practicing in Washington, D.C., described a 50-year-old patient who tested positive, suffered the effects, tested negative twice, then tested positive again with more severe symptoms a second time, about six weeks later:
It is possible, but unlikely, that my patient had a single infection that lasted three months. Some Covid-19 patients (now dubbed “long haulers”) do appear to suffer persistent infections and symptoms.
I believe it is far more likely that my patient fully recovered from his first infection, then caught Covid-19 a second time after being exposed to a young adult family member with the virus. He was unable to get an antibody test after his first infection, so we do not know whether his immune system mounted an effective antibody response or not.
We’ve had these worries earlier this year. Back in early April, South Korean doctors initially believed they were seeing people get sick a second time from “reactivation” of the virus. The Korean CDC initially characterized these cases as “reactivation” of the virus, not reinfection, believing the body fights off the virus for a while, at a sufficient level to make the virus seem dormant, and then the immune system stops fighting it as effectively, causing a second flare-up.
But by the end of the month, the South Korean CDC concluded the patients tested positive a second time “because fragments of the virus remained in their bodies and showed up in test kits.” Apparently, the tests the South Koreans were using were “so sensitive that [they] can still pick up parts of the small amount of RNA from a cell even after the person has recovered from COVID-19.”
An earlier antibody test on Dr. Ackerly’s patient would have been particularly useful in unraveling this mystery. Maybe the patient’s body exhibited something similar to the original South Korean theory — his body fought off almost all of the virus but not quite all of it, enough to test negative. (We should also recognize that some small portion of tests will give inaccurate results. If the tests are 90 percent accurate, wouldn’t one patient out of 100 positive patients generate two false negatives in a row?) With the virus mostly but not entirely gone, the patient’s immune system “relaxes”. . . and eventually, the virus returns with a vengeance, worse the second time because the viruses that survived the first battle are a little tougher and the ones that are best adapted to fight the patient’s immune system.
Or maybe this patient’s immune system is just not that strong. As noted yesterday, a lot of how our body responds to pathogens is determined by our genes, and some human beings hit the jackpot and have immunity or near-immunity to some common health problems. (A small minority of humans are immune to mosquito bites.) In the eyes of the patient, the difference between “reinfection” and “reactivation” is probably moot; in either case, you get sick, you get better, you think you’re in the clear, and then you get sick again.
It is also theoretically possible that this patient encountered a mutated strain of the coronavirus that is too different from the first strain for his body to effectively fight it off. Before you start worrying about that, keep in mind that so far, the only significant mutation of SARS-CoV-2 that researchers have uncovered is one that makes it more contagious, not more deadly or too different for a patient’s immune system to recognize. (Some scientists think the virus might be getting less deadly, but the jury is still out on that, so to speak. A declining rate of death among the infected, like we’re seeing right now, might be because the virus is growing less virulent, but it’s difficult to differentiate that factor from the improvements in treatment and less vulnerable patients getting infected in the current waves.)
As Ed Cara notes, the body’s response to a viral infection utilizes both antibodies and T-cells, which you may have heard of in the context of cancer treatments. T-cells are produced in bone marrow but get their name because they develop in the thymus gland. T-cells are basically the special forces of your immune system and split into two groups. The first, CD8, acts as the Navy SEALS of your immune system: They take on infections, virus bacteria, and tumors and, God willing, take them all down. The second category of T-cells, CD4, are the support staff, performing a variety of duties . . . including the production of cytokines. (Readers who remember past articles about chloroquine and hydroxychloroquine recognize that term from the discussion of the dangers of “cytokine storms” and how that drug can prevent the immune system from overreacting at attacking healthy cells.) Our bodies’ production of T-cells slows after puberty and basically is gone by age 65, which is one reason why elderly people are more vulnerable to infection.
As this Wired article lays out, some new research suggests that bodies with not-so-great antibody levels can still have effective T-cell responses against this virus. The study found SARS-CoV-2-specific CD8 T-cells were found in about 70 percent of recovering patients and 100 percent of patients had CoV-2-specific CD4 T-cells. But also, “importantly, we detected SARS-CoV-2-reactive CD4+ T cells in ∼40 percent –60 percent of unexposed individuals, suggesting cross-reactive T cell recognition between circulating ‘common cold’ coronaviruses and SARS-CoV-2.”
In other words, 40 to 60 percent of people who hadn’t caught the virus yet had T-cells that had been “in training” against regular non-SARS-CoV-2 coronaviruses and that were likely to be effective in fighting off SARS-CoV-2. (Suddenly, asymptomatic cases make a bit more sense. Those folks are probably lucky enough to have immune systems that are top-tier and never let the SARS-CoV-2 virus get enough traction to generate symptoms. Remember, coughs, sneezes, runny noses, and other symptoms of sickness are ways the body is trying to expel the invader.)
The body’s immunity against reinfection from other types of coronaviruses is pretty impressive. Keep in mind: Most of the common colds are coronaviruses; if our bodies couldn’t retain the ability to fight them off, we would keep catching the same cold over and over again throughout the winter. One study of seven Jordanians infected with MERS — Middle East Respiratory System — found that six had antibodies in their system nearly three years later. (That sample may seem small, but remember MERS only infected about 2,500 people total.)
Is Herd Immunity Still Far, Far Away . . . or a Closer Than Most People Think?
Last night, Mississippi governor Tate Reeves offered a clear and succinct series of tweets, laying out why he’s not putting too much hope in “herd immunity” taking effect in his state. He noted that just to reach the threshold of 40 percent infected, the number of infected in his state would have to increase from the roughly 37,000 known infections to about 1.2 million. Are there asymptomatic people walking around Mississippi, unaware they have the virus? Sure. Are there 100,000? Half a million? A million?
Reeves summarizes, “on our worst day of new cases, we had just over 1,000. It has typically been between 700-900 during this most aggressive time. To get to 40% infections, we’d need 3,187 new cases every day for a full year from today. We would need to TRIPLE our worst day — every day — for a year.”
With that said, it is reasonable to believe that certain neighborhoods and communities that were particularly hard hit in the early stages of this pandemic might have reached herd immunity, or something close to it. A of couple days ago, the New York Times reported, “At a clinic in Corona, a working-class neighborhood in Queens, more than 68 percent of people tested positive for antibodies to the new coronavirus. At another clinic in Jackson Heights, Queens, that number was 56 percent. But at a clinic in Cobble Hill, a mostly white and wealthy neighborhood in Brooklyn, only 13 percent of people tested positive for antibodies.” The article cautiously notes that the people who come into the clinic to be tested may not be representative of the neighborhoods as a whole.
New York political leaders are particularly pleased with the declining number of deaths and new cases these days. Yes, this is what happens when the virus has burned through an area so thoroughly — the virus finds fewer and fewer people who don’t have the antibodies.
July 14, 2020 – Florida tops its single-day record for coronavirus deaths, but death rate falls through floor to less than 1%, Chicago Tribune (Commentary)
The Chicago Tribune reports that Florida surpassed its daily record for coronavirus deaths Tuesday amid rising global worries of a resurgence.
Florida’s 132 additional deaths topped a state mark set just last week. The figure likely includes deaths from the past weekend that had not been previously reported.
The new deaths raised the state’s seven-day average to 81 per day, more than double the figure of two weeks ago and now the second-highest in the United States behind Texas.
The worrisome figures were released just hours before the news about the experimental vaccine, developed by the National Institutes of Health and Moderna Inc.
With the virus spreading quickly in the southern and western U.S., one of the country’s top public health officials offered conflicting theories about what is driving the outbreak.
“We tried to give states guidance on how to reopen safely. …If you look critically, few states actually followed that guidance,” Dr. Robert Redfield, the director of the Centers for Disease Control and Prevention said Tuesday in a livestream interview with the editor of the Journal of the American Medical Association.
Redfield said people in many states did not adopt social distancing and other measures because they hadn’t previously experienced an outbreak. But he went on to say, without explanation, that he didn’t believe the way those states handled reopening was necessarily behind the explosive rise in virus cases. He offered a theory that infected travelers from elsewhere in the country might have brought the virus with them around Memorial Day.
CDC officials said that there are various possible explanations, and that Redfield was offering just one.
Doctors in Florida have predicted more deaths as daily reported cases have surged from about 2,000 a day a month ago to a daily average of about 11,000, including a record 15,000 on Sunday. The state recorded 9,194 new cases Tuesday.
Marlyn Hoilette, a nurse who spent four months working in the COVID-19 unit of her Florida hospital until testing positive recently, said hospitals are so desperate for staff to return to work they are not following guidelines that call for two negative tests first.
“Nurses are getting sick, nursing assistants are getting sick and my biggest fear is that it seems we want to return folks to work even without a negative test,” said Hoilette, who works at Palms West Hospital in Loxahatchee. Florida. “It’s just a matter of time before you wipe the other staff out if you’re contagious, so that is a big problem.”
Commentary — you can smell the hysteria in this story — and the hospital staff crisis in Florida appears to be real, as it is everywhere in the U.S. — but the plain fact of the matter is that the Florida daily death toll from coronavirus — while setting a record — is actually microscopic.
We’re looking at a record 132 deaths a day in Florida compared to a record 15,300 new cases a day in Florida. That’s a mortality rate of .8 percent, or less than 1 percent. And significantly, this tremendously important fact is completely ignored by this story.
Overall, as of July 16, 2020, there have been 254,511 COVID-19 infections in Florida, and 4,197 deaths. That’s a death rate of 1.6 percent.
By comparison, there have been between 9 million and 45 million cases of the common flu annually over the last decade in the U.S., with between 12,000 and 61,000 deaths annually from the flu in the U.S., according to the CDC. That’s a mortality rate of 1.3 percent for the common flu.
So despite all the hand wringing, coronavirus in Florida is about as lethal as the common flu, which as everyone knows, IS NO BIG DEAL.
The press in America is all about terrorized hysteria!
June 15, 2020 – How a False Hydroxychloroquine Narrative Was Created, Mercola.com (Commentary)
Dr. Joseph Mercola of Mercola.com details how hydroxychloroquine — a cheap generic drug that has been used successfully against malaria for over half a century, and has recently been used successfully worldwide against COVID-19 — was demonized by the World Health Organization and the British medical publication The Lancet after it was touted by President Donald Trump (although Mercola does not mention Trump once in his article).
Mercola outlines how a WHO study partially funded by the Bill and Melinda Gates Foundation used lethal doses of hydroxychloroquine (“2,400 mg of hydroxychloroquine during the first 24 hours — three to six times higher than the daily dosage recommended”), and then concluded the drug — which has been used safely for decades — was unsafe, and how a study of hydroxychloroquine published in The Lancet — which also dubbed hydroxychloroquine unsafe — had to be quickly retracted for using fabricated data.
Commentary — This is a detailed, highly medical/scientific article which is hard to read, but also important — not just to the political debate in the United States, but also to the treatment of millions of people worldwide who are suffering from COVID-19.
As French science-prize winning microbiologist and infectious disease expert Dr. Didier Raoult, who is also founder and director of the research hospital Institut Hospitalo-Universitaire Méditerranée Infection, said on July 2, 2020, failure to prescribe hydroxychloroquine to a COVID-19 patient “should be grounds for malpractice.”
Yet the mud thrown at hydroxychloroquine and Trump by the WHO and The Lancet has stuck to a considerable degree in the minds of many Americans, especially liberals who reflexively believe anything negative about the President of the United States, and anything that swells the coffers of Big Pharma.
The New York Times writes that some people say we’re doomed. But science and public spending have saved us from pandemics worse than this one.
Nearly 140,000 Americans have been lost to coronavirus, and many experts fear that the deaths will only accelerate in the fall as cold weather forces us indoors. By year’s end, half as many Americans may have died as did in the four years of World War II.
And yet we are still arguing over how to prevent this — each state struggling over how much lockdown to impose and what its governor can make its citizens do.
“You know the five stages of grief — denial, anger, bargaining, depression, acceptance?” asked Dr. Emily Landon, a coronavirus expert at the University of Chicago medical school. “I think the American people are in all five of them — but different parts of the country are in different stages.”
As death stalks us, especially our elders, have we simply become inured to the idea that many of us are doomed?
The stock market appears to have priced in a huge wave of deaths. In the 2008-2009 recession, it fell 50 percent and took four years to recover. In March it fell only 34 percent and has made up much of that ground already. Looked at with Wall Street’s bloodless arithmetic, that makes sense: Most of the deaths are among the very elderly and nursing home residents, who no longer travel or dine out or contribute much to the economy, and who are a burden on the struggling Medicare and Social Security Trust Funds.
One can even argue that the acceptance of death as master of us all is part of the human psyche. But because of modern medicine, we have been out of touch with our ultimate fate for generations.
We’ve all heard of the Black Death and perhaps the Plague of Justinian, events that may have killed up to a third of mankind and rewrote the fates of empires. They seem lost in the mists of time.
But not that long back, our great-great-great-great-grandparents felt the omnipresence of death in ways we will never know.
There is a chart famous among epidemiologists titled “The Conquest of Pestilence in New York City.” Produced by New York City’s health department, it tracks and explains deaths in the city from the early 1800s to the present day.
At first glance, it looks innocuous, like the ups and downs of the Dow Jones index. But the longer you stare at the fine print, the more horrified you become.
This past March, before coronavirus cases began to mount, the annual death rate in New York City was about six per 1,000 New Yorkers. The virus’s first wave added about 2.5 more deaths per 1,000 to that baseline. By contrast, from 1800 into the 1850s, deaths in the city rose in a relentless series of epidemic spikes, year after year, with only brief respites in between.
The annual baseline back then was about 25 deaths per 1,000 New Yorkers, and in some years the toll reached 50 per 1,000. In other words, in bad years, New Yorkers saw twice as many people around them die as usual. And they were used to seeing about four times as much death as we now do.
The sharpest peaks were the cholera epidemics of 1832, 1849 and 1854. But plagues came in waves, sometimes more than one simultaneously: yellow fever, smallpox, measles, scarlet fever, diphtheria, typhus and meningitis.
Other than cholera and typhus, most of those were childhood diseases that adults were immune to because they had survived them, so the chart is a parabola of parental grief, each spike another nail in a hundred small coffins.
The death rate began dropping after the 1860s. New Yorkers — both citizens and doctors — had finally stopped arguing and reached consensus on some basic issues.
First of all, most finally accepted the “germ theory” of disease, acknowledging that it was caused by invisible enemies, not by swamps, trash, manure or the other nuisances that underlay the “miasma theory,” which held that bad smells caused disease. (Only a century earlier, Americans had given up on the “humors theory,” which posited that disease was caused by imbalances among blood, urine, sweat and bile that had to be rebalanced by bleeding, sweating or purging.)
They also agreed that whether immigrants had brought some diseases or simply suffered from them, no one was safe until everyone was safe, so they made public health universal.
As a result, New Yorkers took certain steps — sometimes very expensive and contentious, but all based on science: They dug sewers to pipe filth into the Hudson and East Rivers instead of letting it pool in the streets. In 1842, they built the Croton Aqueduct to carry fresh water to Manhattan. In 1910, they chlorinated its water to kill more germs. In 1912, they began requiring dairies to heat their milk because a Frenchman named Louis Pasteur had shown that doing so spared children from tuberculosis. Over time, they made smallpox vaccination mandatory.
Libertarians battled almost every step. Some fought sewers and water mains being dug through their properties, arguing that they owned perfectly good wells and cesspools. Some refused smallpox vaccines until the Supreme Court put an end to that in 1905, in Jacobson v. Massachusetts.
In the Spanish flu epidemic of 1918, many New Yorkers donned masks but 4,000 San Franciscans formed an Anti-Mask League. (The city’s mayor, James Rolph, was fined $50 for flouting his own health department’s mask order.) Slowly, science prevailed, and death rates went down.
Today, Americans are facing the same choice our ancestors did: We can listen to scientists and spend money to save lives, or we can watch our neighbors die.
“The people who say ‘Let her rip, let’s go for herd immunity’ — that’s just public-health nihilism,” said Dr. Joia S. Mukherjee, the chief medical office of Partners in Health, a medical charity fighting the virus. “How many deaths do we have to accept to get there?”
A vaccine may be close at hand, and so may treatments like monoclonal antibodies that will cut our losses.
Till then, we need not accept death as our overlord — we can simply hang on and outlast him.
Commentary — THIS IS A silly and slight “think piece” that inadvertently reveals several things it does not intend or comprehend.
The first is how much the belief system of secular liberals resembles the belief system of Christian conservatives.
Both secular liberals — for whom the New York Times is frequently taken as a sort of Holy Book of Truth — and devout Christian conservatives believe humanity will be saved from this great coronavirus crisis by a higher, external force outside their everyday lives.
For Christians, it is the hand of almighty God. For secularists, it is the hand of almighty Science.
So the author of this piece (“Your Ancestors Knew Death in Ways You Never Will”), Donald G. McNeil Jr., contends that “science and public spending have saved us from pandemics worse than this one,” and it will save the day this time too. Although certainly comfortable enough as platitudes go, this statement is simply not true, nor does McNeil understand what “saved us” from past pandemics.
Here’s the matter of pandemics put simply. Every single pandemic that has afflicted the human species — from before the beginning of recorded history until now — has been been overcome and ended by a very simple behavioral and biological processes that are evident every day in the lives of human beings everywhere, and many other higher species on Earth as well.
These simple, every day processes produce cultural behavior and aggregate genetic movement toward what we now call “herd immunity,” meaning sufficient immunological resistance to a given microbial attacker so that the population is no longer susceptible to wildfire-like pandemics.
True, both religion and science can play a supporting role in the natural movement toward herd immunity. Religion can give people emotional strength, which is important because people’s emotions play such an big role in every struggle they face. And science likewise can play an important supporting role, especially if a vaccine can be created, since a vaccine can accelerate the species’ movement toward herd immunity, and save lives that would otherwise be lost in what remains a bitter battle to achieve herd immunity against COVID-19.
But neither religion nor science is the prime mover or the root cause here. The process that ends pandemics is natural, is with us every day, and has been with us as long as there have been human beings on earth. This is something that should make people everywhere on the earth feel good about our prospects in the battles to come, and proud and easy in their humanity .
The process has three parts — (1) the natural physical development of immunity through antibodies, T-Cells, immune system “dark matter,” and the other known and unknown natural processes of our physical bodies that fight invasive, infectious diseases, and (2) broad but not universal changes in human behavior (the species always hedges its bets) that increase herd immunity, and (3) the death of the weakest members of the populations who are tinder for the pandemic firestorm.
So a society with many weak members, and nursing homes full of the elderly, the injured and the brain dead, America was primed for a pandemic as 2020 dawned. It was like a dry California forest in the summer with a lot of dry dead branches and assorting underbrush lying on the ground because management authorities stopped the natural burning process, and created super fires for their trouble — the forest fire equivalent of a pandemic.
A profound irony of pandemics is that they make the human species strong and vital — physically, emotionally and intellectually. We — human beings as a species– will be a stronger, more competitively capable species when this pandemic is over than we are now. Coronavirus is like the wolf pack that cleans the caribou herds and keeps them strong by killing the weak.
LET’S TAKE A look at New York plagues of the past, and the number of people they killed. These are plagues that this Times editorial says have been ended by “science and public spending.” Among others, we find the:
- Yellow fever epidemic of 1805, 270 people died in New York
- Small pox epidemic of 1824, 394 people died in New York
- Cholera epidemic of 1834, 3,053 people died in New York
- Cholera epidemic of 1854, 5,071 people died in New York
- Diptheria epidemic of 1887, 4,509 people died in New York
- Meningitis epidemic of 1904, 2,219 people died in New York
- Spanish influenza epidemic of 1918, 12,562 people died in New York
There were no vaccines for any of these diseases at the time of the New York epidemics listed above, so each of them flared and then burned through America’s largest city for as long as long and hard as herd immunity would let them, and they finally burned out as a super fire when easy or weak victims had been killed, and selectively eliminated.
Changes in human behavior during plagues frequently affect herd immunity for the species too, both for and against. In A Journal of the Plague Year, Daniel Defoe (of Treasure Island fame) describes how residents of London became highly concerned with the cleanness of the air they breathed with others during the Plague of 1665 (just like with COVID-19 today), so they fled the cities (just like with COVID-19 today), thereby spreading the plague to remote areas outside the cities (just like with COVID-19 today).
Defoe also describes what we today call asymptomatic carriers:
“I mean such as had received the contagion, and had it really upon them, and in their blood, yet did not show the consequences of it in their countenances: nay, even were not sensible of it themselves, as many were not for several days. These breathed death in every place, and upon everybody who came near them; nay, their very clothes retained the infection, their hands would infect the things they touched, especially if they were warm and sweaty, and they were generally apt to sweat too.
Now it was impossible to know these people, nor did they sometimes, as I have said, know themselves to be infected…
Defoe also describes increasingly stringent but not always effectual laws enacted by the City of London to try to stop the spread of the contagion (just like with COVID-19 today). Londoners in 1665 were fully alive to the threat of airborne, aerosol infection, just people are today with the COVID-19 masks that many people are required to wear now. In 1665, Defoe wrote of how the Bubonic plague spread by “mutual respiration”:
Contagion is the inseparable symptom of the plague; which, by mutual respiration, is transfused from the infected persons to the lungs and stomach of those who approach them.
AND THERE ARE also echoes of what we’re experiencing today in the annals of the ancient world. During the so-called Justinian plague that struck Europe in 541 AD, during the reign of Roman Emperor Justinian, the functioning of the Roman Empire was significantly disrupted by the Bubonic plague, Yersinia pestis. Justinian himself was sickened, but recovered. Modern medical research has established that the strain of Bubonic plague that wasted the last years of Justinian’s reign had originated in China (just like with COVID-19 today).
And nearly a millennia before Justinian, Greek philosopher Socrates was said by Edward Gibbon in The Decline and Fall of the Roman Empire to have lived through the plague that struck Athens during the second year of the Peloponnesian War (430 BC) by virtue of his “temperance.”
Ancient Greek physicians argued about whether a recovered plague patient could be reinfected with the plague — in other words, whether plague survivors achieved strong immunity against re-infection (just like with COVID-19 today). Thucydides argued that plague survivors acquired immunity, while Gibbons wrote that “Evagrius, who had family experience of the plague, observes, that some persons, who had escaped the first, sunk under the second attack; and this repetition is confirmed by Fabius Paullinus.”
THE ONLY REASON I mention all this is to demonstrate that the chaotic behavior we’ve seen in the global reaction to the COVID-19 pandemic during it’s first six months is just fine.
So you say the government didn’t get a good handle on the situation at the outset, when it could have made a big difference? Don’t worry about it. It’s scripted that way, and that’s exactly how human pandemic dramas have played out, over and over again.
THIS IS HOW HUMAN BEINGS ACT WHEN A PANDEMIC CONFRONTS THEM. It’s been going on for thousands of years beyond counting. It’s how we get the job done, as a species. It’s how we survive.
Please note, however. There was never a vaccine against any of these ancient plagues of ancient Greece and Rome, as there was no vaccine for Defoe’s London plague of 1665, which is also the plague that produced Der Doctor Schnabel von Rom (“Doctor Nose of Rome”).
Science as we know it today did not even exist, and was not a factor at all in these stories. Here, the natural bio/behavioral process of creating herd immunity overcame every plague threat naturally.
Sometimes the human cost of combing out the weak undercoat of humanity was considerable, and authentically tragic. But the species has come through every single plague threat it has ever faced, and come through stronger. As with the arctic caribou and the wolf, we do better as a species when our weakness is combed out.
FINALLY, I must concede that New York Times science reporter Donald G. McNeil Jr. is correct in one respect — public spending has played a role in the history of human plagues.
In Defoe’s time, the City of London and other afflicted cities of Europe undertook modest public expenditures to control the disease’s spread, which began with burying the dead, a public minded act that immediately increased taxes since the citizens of London were levied a burial tax to pay for the monthly public expenditures to bury the dead.
The City of London’s next recourse, according to Defoe, was to lock anyone diagnosed with the plague and their entire family in one house together under lock and guard, which could amount to a death sentence for anyone diagnosed and anyone they had contact with, when it was strictly enforced, which it sometimes was.
A thousand years before, in the nearly decade long era of the Justinian plague, the Romans still had the scope and power to levy and expend in quantities that might meet a stricter definition of “public expenditure.” And Emperor Justinian did expend, although mostly for bureaucracy to try to maintain the pre-plague tax flow to Imperial coffers, so that — according to the Gibbon — the living were liable for their own tax obligation, as well as the tax obligation of their plague deceased neighbors.
And yet the human species survived, thrived, conquered new and unimagined realms like never before. So there’s no need to fear the wolf, which for us is coronavirus.
We need the wolf to make us strong and successful, and I’ll say it again — we are going to come out of this pandemic a stronger species than we were going in.
July 16, 2020 – The coronavirus pandemic most resembles the the 1957 Asian flu pandemic, Coronavirus Vaccine & Herd Immunity Digest
The Coronavirus Vaccine & Herd Immunity Digest writes that the coronavirus pandemic has most frequently been compared to the 1919 Spanish influenza pandemic, which was the most deadly flu epidemic in history.
The CDC estimates that 675,000 people died from the Spanish influenza in the United States, and a 2006 CDC article says the Spanish influenza’s case fatality rate was around 2.5%, which means 2.5 percent of people infected died, although both the death rate and the total number of deaths may have been much higher.
By comparison, there have been 138,000 death attributed to COVID-19 to date, and the COVID-19 mortality rate was recently calculated by the New York Times at 0.6 percent, or about 1/2 or 1 percent, meaning 1/2 of 1 percent of those infected may be expected to die.
So both the total death count and the death rate attributed to the coronavirus pandemic are far, far lower than those observed with the Spanish influenza, which was a more potent killer than COVID-19 by all measures.
What then can COVID-19 be meaningfully compared to? How about the Asian flu?
Both the coronavirus and the Asian flu are novel coronaviruses which apparently crossed over to humans from non-human species. In the case of the Asian flu, the origin was the H2N2 avian flu (possibly from geese), and both pandemics came out of China. The Asian flu first appeared in Guizhou, China, in late 1956, then in Singapore and Hong Kong in the spring of 1957.
In terms of mortality rate, the COVID-19 and Asian flu pandemics are very similar. Like COVID-19, the Asian flu had a human mortality rate of a little more than 1/2 of 1 percent. “The case fatality rate of Asian flu was approximately 0.67%,” according to Wikipedia.
The estimated number deaths attributed to the Asian flu and coronavirus are somewhat comparable as well. There were 116,000 Asian flu deaths in the United States, according to the CDC, compared to 138,000 deaths from COVID-19 in the U.S. to date. (Because the population of the Unites States was much smaller in 1957, the Asian flu actually killed a larger percentage of the American population than COVID-19 has so far.)
And like COVID-19, the Asian flu hit the elderly hardest and was most deadly for that portion of the population.
There are, however, two big differences between the Asian flu and COVID-19 stories. The first is that the U.S. was able to have a vaccine ready by the fall of 1957, when the Asian flu hit America.
The other difference is that no one gave even a moment’s thought to closing the whole country down for the Asian flu pandemic, even though its mortality rate and death count were similar to the coronavirus pandemic.
There was no heavy-breathing hysteria in America in 1957. People just took the best precautions they could, and got on with it.
French virologist Luc Antoine Montagnier, who was awarded a Nobel prize in Physiology in 2008 along with Françoise Barré-Sinoussi and Harald zur Hausen for discovering of the HIV virus, says COVID-19 is manmade.
Appearing on the French cable TV show, CNews, on April 17, 2020, Luc Antoine Montagnier stated that the virus that causes COVID-19 is manmade, and that elements of HIV and Plasmodium falciparum, a parasite that causes malaria, are found in the coronavirus’s genome.
“We were not the first since a group of Indian researchers tried to publish a study which showed that the complete genome of this coronavirus [has] sequences of another virus, which is HIV.”
The research that Montagnier refers to was posted on the science website Biorxiv January 31, 2020, and has since been withdrawn. The Indian researchers wrote:
“We found 4 insertions in the spike glycoprotein (S) which are unique to the 2019-nCoV and are not present in other coronaviruses. Importantly, amino acid residues in all the 4 inserts have identity or similarity to those in the HIV-1 gp120 or HIV-1 Gag …
The finding of 4 unique inserts in the 2019-nCoV, all of which have identity /similarity to amino acid residues in key structural proteins of HIV-1 is unlikely to be fortuitous in nature.”
Montagnier says COVID-19 Derives From a Failed HIV Vaccine.
In a separate appearance on the French podcast Pourquoi Docteur, also April 17, Montagnier said the coronavirus had escaped in an “industrial accident” while Chinese scientists at the Wuhan city laboratory were trying to develop a vaccine against HIV. “In order to insert an HIV sequence into this genome, molecular tools are needed, and that can only be done in a laboratory,” said Montagnier.
Montagnier also said he believes that the pandemic will naturally extinguish itself because of its synthetic origins:
“Nature does not accept any molecular tinkering, it will eliminate these unnatural changes and even if nothing is done, things will get better, but unfortunately after many deaths.”
According to the website Corvelva, Montagnier said on the podcast that the pandemic would peter out because nature would override the synthetically inserted sequences that make COVID-19 so deadly:
Montagnier says he reached his conclusions, “With my colleague, biomathematician Jean-Claude Perez,” after they “carefully analyzed the description of the genome of this RNA virus.” Montagnier’s partner, Perez, is a French interdisciplinary scientist and biomathematics expert.
In a paper Montagnier and Perez published by the Center for Open Science in April 2020, they write:
“Using our proprietary bio-mathematic approach we are able to evaluate the level of cohesion and organization of a genome; … we then searched in this genome for possible traces of HIV or even SIV [related simian immunodeficiency virus]. A first publication reports the discovery of 6 HIV SIV RNA pieces.”
The HIV and SIV elements that Montagnier and Perez detect, called Exogenous Informative Elements, or EIEs, provide the basis of their theory that COVID-19 is not a simple derivative of SARS and bat-related viruses. They write:
“A major part of these 16 EIE already existed in the first SARS genomes as early as 2003. However, we demonstrate how and why a new region including 4 HIV1 HIV2 Exogenous Informative Elements radically distinguishes all COVID-19 strains from all SARS and Bat strains …
… a contiguous region representing 2.49% of the whole COVID-19 genome is 40.99% made up of 12 diverse EIE originating from various strains of HIV SIV retroviruses …
a novel long region of around 225 nucleotides, appears to us to be totally new: this region is completely absent in ALL SARS genomes, whereas it is present and 100% homologous for all COVID-19 genomes listed in NCBI or GISAID COVID_19 genomic databases.”
In June 2020, research published in the Quarterly Review of Biophysics makes similar claims. Norwegian scientist Birger Sørensen and British oncologist Angus Dalgleish refer to COVID-19 as a “chimeric virus” and write:
“We show the non-receptor dependent phagocytic general method of action to be specifically related to cumulative charge from inserted sections placed on the SARS-CoV-2 Spike surface in positions to bind efficiently by salt bridge formations; and from blasting the Spike we display the non human-like epitopes from which Biovacc-19 has been down-selected.”
While conceding the Quarterly Review of Biophysics assertions were controversial, the scientific website Minerva wrote that the science should be pursued.
“Minerva has read a draft of the article, and has after an overall assessment decided that the findings and arguments do deserve public debate, and that this discussion cannot depend entirely on the publication process of scientific journals.”
Commentary — if you’re wondering why you haven’t heard this before, the reason is that these highly significant comments by a distinguished scientist in the field have been completely ignored by the American press.
July 18, 2020 – State Department releases cable that launched claims that coronavirus escaped from Chinese lab, Washington Post (Commentary)
The State Department has released an internal cable from 2018 detailing the concerns of U.S. Embassy officials in China about a lack of adequately trained personnel at a virology lab in Wuhan, the city that later became the epicenter of the novel coronavirus outbreak.
Leaked contents of the cable sparked unproven speculation from senior U.S. officials beginning in April that the outbreak occurred as a result of an accident at the Wuhan Institute of Virology.
In May, President Trump said he had seen evidence that gave him a “high degree of confidence” that the coronavirus originated in a Chinese lab. When asked why he was confident, Trump said, “I can’t tell you that. I’m not allowed to tell you that.”
The full cable does not strengthen the claim that an accident at the lab caused the virus to escape, nor does it exclude the possibility. However, in recent months, skepticism of the accident theory has increased in the scientific community because the genetic sequences of isolates from the bat coronaviruses known to be under research at the lab do not match those of covid-19.
The State Department cable says the lab, which U.S. officials visited in 2018, “has a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory.”
It also says that scientists in the lab were allowed to study SARS-like coronaviruses isolated from bats but were precluded from studying human-disease-causing SARS coronaviruses in their lab unless given explicit permission from a designated commission.
When asked on Friday whether he had evidence supporting the lab theory beyond the 2018 memo, a spokesperson did not point to a specific of piece of information but offered Pompeo’s remarks from Wednesday calling on China to be transparent.
“They have destroyed samples; they’ve taken journalists and doctors who were prepared to talk about this and not permitted them to do what nations that want to play on a truly global scale and global stage ought to do: be transparent and open and communicate and cooperate,” Pompeo said
The Office of the Director of National Intelligence has not endorsed or refuted the lab theory. In May, it issued a statement saying intelligence officials were still examining whether the virus “began through contact with infected animals or if it was the result of an accident at a laboratory in Wuhan.”
Commentary — There is a significant omission in this story which seriously slants it.
The Post states, “skepticism of the accident theory has increased in the scientific community because the genetic sequences of isolates from the bat coronaviruses known to be under research at the lab do not match those of covid-19.”
Is it possible that the Washington Post is unfamilar with the recent comments of distinguished French virologist Luc Antoine Montagnier? Montagnier, who was awarded a Nobel prize in Physiology in 2008 for his work identifying HIV, has said his research indicates that COVID-19 has been genetically engineered, and is manmade.
This comment from a highly respected scientist in the field not only lends credence to President Trump’s claim, it explains WHY the COVID-19 form of the virus doesn’t perfectly match Wuhan Lab sample RaTG13 — namely that COVID-19 has been genetically engineered from a naturally occuring coronavirus.
Furthermore, as the Times of London has reported, the Wuhan Institute of Virology (WIV) has acknowledged that it was performing “gain-of-function” genetic alterations on viruses to increase their virility, and make them more infectious to human beings. So we know that the Chinese were in fact performing genetic engineering on coronavirus specimens in their posession!
According to the Times of London:
This “gain-of-function” work is described in papers released by the WIV between 2015 and 2017, scientists say. Shi’s team combined snippets of different coronaviruses to see if they could be made more transmissible in what they called “virus infectivity experiments”.
Does the Washington Post think Nobel Laureate Luc Antoine Montagnier is not a member of the “scientific community”?! And is the Post unaware that the WIV was performing “gain-of-function” genetic engineering on the coronavirus specimens it had collected?!
Or maybe the Post is just willfully ignorant of these facts because they don’t fit its political agenda?
July 21, 2020 — Study says actual number of Covid-19 cases is far greater than thought, CNN, (Commentary)
CNN reports that the number of people who have had Covid-19 is much greater than the official case count, according to data and a new analysis released by the US Centers for Disease Control and Prevention on Tuesday. Depending on the region and the time period, the number of people infected was anywhere between 2 and 24 times the number of reported cases, the CDC team said.
“For most sites, it is likely that greater than 10 times more … infections occurred than the number of reported Covid-19 cases,” the team wrote. In New York, the CDC estimates suggest that 642,000 people were infected by April 1 but at that point only 53,803 cases were officially reported. That means the number of infections could be at least 12 times higher than reported, the CDC said.
The CDC says the number of cases in South Florida, Connecticut and Minnesota was 6 to 11 times higher than the official count, the CDC said.
These numbers are likely conservative, according to the study in the Journal of the American Medical Association. The data used in the analysis was published on the CDC website.
The CDC has updated that data since the report was submitted to show two different testing periods starting in March and April. CDC Director Dr. Robert Redfield said last month that testing had likely missed 90% or so of cases. The country remains far from a level that would give the population herd immunity — assuming that having been infected once provides immunity. Doctors are not sure if that is the case.
Hours after the CDC analysis was released, President Donald Trump warned Americans that the pandemic will “probably, unfortunately, get worse before it gets better.”
Commentary — Sometimes good news comes in strange forms, and this is one of them.
This story is old news to anyone who has contacts in the medical field. The nurses I know have been saying for months that the official COVID-19 infection and death counts are way too low.
Now the CDC has officially concured with the nurses in the wards.
In New York City, for instance, the CDC now thinks the infection rate was 12 times greater than reported at the time. Stated another way, that means that the CDC missed more than 90 percent of the coronavirus cases this spring.
In New York City, this would mean there were 642,000 people infected by COVID-19 by April 1, not the paltry 53,803 infections that were officially reported at the time.
So how is this good news, you ask? It’s fabulous, dance-in-the-streets good news because it means that many, many more people than originally thought will now been exposed to COVID-19, and thrown it off, many of them without even knowing they were sick!
Not only have these heros of the pandemic demonstrated innate, inheritted strength against the disease, they now have some form of devloped immunity against COVID-19. We’re not sure exactly what yet, — but it will likely be expressed in the form of antibodies, T-cells, and possibly “immunological dark matter,” and it will convey SOME kind of increased immunity to COVID-19 because the people who threw off COVID-19 sight-unseen have now seen it before.
And this is EXACTLY what we’ve got to do to beat this pandemic — we’ve got to get the population to the herd immunity point, where enough people are immune that the disease can’t flare to wildfire proportions. This is how humanity has beatten every plague that’s ever challenged it, and it’s how humanity will beat this plague too, with or without a vaccine.
One true ray of good news on the coronavirus pandemic front right now are reports indicating that the hardest hit neighborhood in NYC have attained herd immunity, with more than 60 percent of the population tested showing antibodies to COVID-19, according to the New York Times.
A recent article in the Atlantic noted of New York:
Essentially, at present, New York City — which was hit very hard by the first coronavirus wave — might be said to be at a version of herd immunity, or at least safe equilibrium. Our case counts are very low. They have been low for weeks. Our antibody counts mean that a not-insignificant number of people are effectively removed from the chain of transmission.
However, the very idea of herd immunity is pretty upsetting for CNN, which ran an OpEd piece as a purported news story two weeks ago under the looney toones headline: “We’re wasting time talking about herd immunity” — never mind that herd immunity is the only path out available to us right now!
So this CNN COVID-19 story quickly and blandly looks past the good herd immunity news from New York, and reassures the reader that:
The country remains far from a level that would give the population herd immunity — assuming that having been infected once provides immunity. Doctors are not sure if that is the case.
Wheh! What a relief.
July 27, 2020 — Two American coronavirus vaccines begin the last phase of testing: 30,000-person trials, Washington Post, (Commentary)
The Washington Post reports that at 6:45 a.m. Monday, a volunteer in Savannah, Ga., received a shot in the arm and became the first participant in a massive human experiment that will test the effectiveness of an experimental coronavirus vaccine candidate. The vaccine is being developed by the biotechnology company Moderna in collaboration with the National Institutes of Health.
The vaccination marks a much-anticipated milestone: the official launch of the first in a series of large U.S. clinical trials that will each test experimental vaccines in 30,000 participants, half receiving the shot and half receiving a placebo. Pharmaceutical giant Pfizer also announced it was initiating a 30,000-person vaccine trial, at 120 sites globally.
“We are participating today in the launching of a truly historic event in the history of vaccinology,” Anthony S. Fauci, director of the National Institute of Allergy and Infectious Diseases, said at a news conference. He noted that the United States has never moved faster to develop a vaccine, from basic science to a large Phase 3 trial designed to test safety and effectiveness.
Fauci predicted that researchers would probably be able to tell whether the Moderna vaccine was effective by November or December, although he explained that it was a “distinct possibility” an answer could come sooner. Pfizer officials have said the company expects to be able to seek regulatory authorization or approval by October.
Company and government officials repeatedly underscored that although the vaccine development effort is moving at record-breaking speed, safety is not being sacrificed.
“There is no compromise at all, with regard to safety, nor of scientific integrity,” Fauci said.
Both vaccines require two doses, spaced several weeks apart. Then researchers will have to wait to see whether people get infected or sick from the novel coronavirus. What they hope to witness is a clear benefit: fewer infections in people who received the vaccine, or less severe episodes of covid-19, the disease caused by the coronavirus. There are many unknowns about how long it could take to see a clear signal of success or failure — including how fast the trials will recruit participants and how long it takes for enough people to become infected to observe whether there is an effect.
Statisticians have been crunching the numbers to predict how many infections would need to occur in the study population to gauge the vaccine’s effectiveness. To show the Moderna vaccine is 60 percent effective, Fauci said, there would need to be about 150 infections among the 30,000 participants.
The trials are also the biggest test yet of a promising technology that has never been approved for use outside medical research. Either vaccine could become the first in a new class of medicines. The vaccines deliver a snip of genetic material that carries the blueprint for the spiky protein that dots the surface of the coronavirus. After a person is vaccinated, their cells will follow the genetic instructions to build the proteins, and their immune systems, confronted with the spike protein, learn how to recognize and mount a defense to the virus without ever being infected.
Commentary — wow, it’s really exciting to see how excited everyone is about this exciting news, and all the exciting experimental whiz bang medical technology that’s gone into the exciting press release, er, story in the Post by Carolyn Y. Johnson!
Since the Russians completed human trials on a COVID-19 vaccine nearly a month ago, it’s interestingly, that the Post story makes no mention of the Russian vaccine candidates, even though the race for a coronavirus vaccine is the biggest American / Russian technology faceoff since Sputnik!
And speaking of Sputnik, 1957 (the year the Soviets lauched Sputnik 1 into orbit around the earth), was also the year that another deadly viral pandemic swept out of China, namely the Asian flu pandemic.
Like COVID-19, the Asian flu was another novel coronavirus that may have crossed the species lines to become infective to humans. The Asian flu had a mortality rate very similar to COVID-19 and killed nearly 120,000 Americans in 1957-58, a far larger percentage of the total American poplation than COVID-19 has killed so far in 2020.
The big difference between the Asian flu in 1957 and the coronavirus in 2020 is that the United States was able to develop and distribute an effective vaccine within six months of the first international outbreak of the Asian flu in Singapore and Hong Kong.
So if the American immuneological experts were as sharp today as the Russians, of even as good as the Americans were nearly 100 years ago, they’d have delivered an effective vaccine and begun distribution LAST MONTH!
When you look at it that way, it kind of makes Modena and Pfizer look like vaccine wannabe chumps, doesn’t it? But of course, the final judgement isn’t in yet on this little matter of a coronavirus vaccine, either way.
And what was Carolyn Y. Johnson thinking when she wrote in her best talking head video news on the scene prose:
Company and government officials repeatedly underscored that although the vaccine development effort is moving at record-breaking speed, safety is not being sacrificed.
“[R]ecord breaking speed”? Only if you ignore what the Russians did a couple weeks ago and what America could do in 1957.
Still, I have to say — Carolyn Y. Johnson is such an exciting young talent!!!