Coronavirus

[Raven-Knightly]

(New York Times, June 27, 2020):

“Actual Coronavirus Infections Vastly Undercounted, C.D.C. Data Shows -
The prevalence of infections is more than 10 times higher
than the counted number of cases in six regions of the United States.”

The number of coronavirus infections in many parts of the United States is more than 10 times higher than the reported rate, according to data released on Friday by the Centers for Disease Control and Prevention. The analysis is part of a wide-ranging set of surveys started by the C.D.C. to estimate how widely the virus has spread. … “This study underscores that there are probably a lot of people infected without knowing it, likely because they have mild or asymptomatic infection,” said Dr. Havers, who led C.D.C. study. “But those people could still spread it to others.”

… The numbers indicate that even in areas hit hard by the virus, an overwhelming majority of people have not yet been infected, said Scott Hensley, a viral immunologist at the Univ. of Pennsylvania who was not involved in the research. "Many of us are sitting ducks who are still susceptible to second waves,” he said.

The difference between recorded infections and the actual prevalence in the data was highest in Missouri, where about 2.65 percent of the population was infected with the virus as of April 26, although many people might not have felt sick. This number is about 24 times the reported rate: nearly 162,000 compared with the 6,800 thought to have been infected by then. The results confirm what some scientists have warned about for months: that without wider testing, scores of infected people go undetected and circulate the virus. …

… Dr. Robert Redfield, the director of the C.D.C., hinted at this trend on Thursday during a call with reporters. “Our best estimate right now is for every case reported there were actually 10 other infections,” Dr. Redfield said. The source for his claim was unclear at that time. The C.D.C. later posted the data on its website and on MedRxiv, a repository for scientific results … not yet … vetted by peer review.

The referenced paper (June 26, 2020):

“Seroprevalence of Antibodies to SARS-CoV-2 in Six Sites in the United States, March 23-May 3, 2020”

[Raven-Knightly]

(The Guardian, June 28, 2020):

“The coronavirus ‘long-haulers’ show how little we still know -
My Covid-19 symptoms lasted for months.
As an infectious disease specialist, I know the importance of widespread testing”

During the early stages of the outbreak, I came down with mild Covid-19-like symptoms. … I became what we now call a Covid-19 “long-hauler” - a patient with initially mild symptoms of likely Covid-19, who would go on to experience a range of sometimes severe symptoms for a prolonged period of time.

The Covid Symptom Study, undertaken by King’s College London, has revealed that 10% of all Covid-19 patients report symptoms for at least three weeks. Surprisingly, people in this so-called Covid tail are on average younger. Most report having been previously healthy, and show relatively mild symptoms in the initial phase of illness. But they continue to experience symptoms such as fatigue, headache, cough, shortness of breath, chest pain, increased heart rates and gastrointestinal and neurological symptoms for weeks or even months following the initial symptoms; often these symptoms might come and go repeatedly.

Though physically I still struggle with lung problems, as a doctor and a scientist I struggle mostly with the lack of knowledge about this condition. We currently have no understanding at all of the biological mechanisms causing these prolonged symptoms. Theoretically, they may be the result of ongoing or resurgent viral replication - which would be important to know since this would imply prolonged infectiousness as well. Perhaps, however, as observed in more severe cases of coronavirus, the virus may trigger an aberrant immune response, resulting in ongoing inflammation throughout the body, which may last far beyond clearance of the virus. A third alternative, as observed commonly following bacterial pneumonia, is that the coronavirus causes more extensive damage of lungs, heart and other organ systems than suggested by the initial symptoms, which simply requires more time to recover.

Without this knowledge, we don’t know if long-haulers are infectious for prolonged periods, or whether they are at risk of experiencing severe complications, and certainly not whether treatment might reduce the duration of their problems. Left unattended, these patients may even develop irreversible damage leading to chronic illnesses.

Until we develop this medical and scientific knowledge, healthcare professionals won’t have the guidance needed to treat these long-haulers. … a high number of long-haulers have organised themselves in online peer support groups. Depending on the country of origin, many report not having received any medical support during their illness, or being dismissed repeatedly. Others report being brushed off by healthcare professionals, misdiagnosed and in receipt of conflicting advice. They also experienced a wide range of stigma - friends keeping their distance for fear they might be infectious, sympathy draining because they “should” have recovered by now, employers losing patience with number of days taken off work.

[Raven-Knightly]

(Washington Post, June 29, 2020):

“This coronavirus mutation has taken over the world.
Scientists are trying to understand why.”

When the first coronavirus cases in Chicago appeared in January, they bore the same genetic signatures as a germ that emerged in China weeks before. … A change in the virus was appearing again and again. This mutation, associated with outbreaks in Europe and New York, eventually took over the city. By May, it was found in 95 percent of all the genomes Ozer sequenced. … Of the approximately 50,000 genomes of the new virus that researchers worldwide have uploaded to a shared database, about 70 percent carry the mutation, officially designated D614G but known more familiarly to scientists as “G.” …

… At least four laboratory experiments suggest that the mutation makes the virus more infectious, although none of that work has been peer-reviewed. Another unpublished study led by scientists at Los Alamos National Laboratory asserts that patients with the G variant actually have more virus in their bodies, making them more likely to spread it. The mutation doesn’t appear to make people sicker, but a growing number of scientists worry that it has made the virus more contagious. …

… Studying both versions of the gene using a proxy virus in a petri dish of human cells, Choe and her colleagues found that viruses with the G variant had more spike proteins, and the outer parts of those proteins were less likely to break off. This made the virus approximately 10 times more infectious in the lab experiment. The mutation does not seem to lead to worse outcomes in patients. Nor did it alter the virus’s response to antibodies from patients who had the D variant, Choe said, suggesting that vaccines being developed based on the original version of the virus will be effective against the new strain. … the New York team offers a different explanation as to why the variant is so infectious. Whereas Choe’s study proposes that the mutation made the spike protein more stable, Sanjana said experiments in the past two weeks, not yet made public, suggest that the improvement is actually in the infection process. He hypothesized that the G variant is more efficient at beginning the process of invading the human cell and taking over its reproductive machinery. Luban, who has also been experimenting with the D614G mutation, has been drawn to a third possibility: His experiments suggest that the mutation allows the spike protein to change shape as it attaches to the ACE2 receptor, improving its ability to fuse to the host cell. …

… Although these experiments are compelling, they’re not conclusive, said Kristian Andersen, a Scripps virologist not involved in any of the studies. The scientists need to figure out why they’ve identified different mechanisms for the same effect. All the studies still have to pass peer review, and they have to be reproduced using the real version of the virus.

[Raven-Knightly]

(Vox, June 29, 2020):

“What a controversial face mask study says about science in the Covid-19 era -
A Nobel Prize winner coauthored a study in a major journal.
More than 40 researchers want it retracted.”

A high-profile dispute between researchers over a study on the role of face masks in preventing Covid-19 is revealing the tensions in how science is conducted during a global pandemic. …

… The study examined how Covid-19 spreads through the air and found that “wearing of face masks in public corresponds to the most effective means to prevent interhuman transmission.” While the authors are not epidemiologists, Nobel Prize-winning atmospheric chemist Mario Molina is among its authors. The finding that masks are a good way to slow the pandemic aligns with other research, as well as the guidance from health agencies that now recommend wearing them. But the idea that they’re the “most effective means” to do so, compared with tactics like social distancing, banning large gatherings, and closing businesses, is a controversial claim. And the scientists calling for a retraction say the evidence presented doesn’t back it up; they found serious flaws with the study’s methodology and some of its underlying assumptions. …

… The PNAS study looked at the number of confirmed cases of Covid-19 from January 23, 2020, to May 9, 2020, with a focus on Italy, New York City, and Wuhan, China, the epicenters of the outbreak. The authors tracked how cases rose and fell, comparing those changes to when policies like lockdowns went into effect. In particular, the authors examined how cases fell when governments issued orders to wear face masks. … Based on these results, the authors concluded that wearing face masks in conjunction with testing, tracing, and isolation is the most viable way to stop the Covid-19 pandemic without a vaccine. …

… The finding that face masks are the most effective way to limit the spread of the virus could be true, and it aligns with numerous other studies on Covid-19 transmission. … In the case of the Zhang et al. study, it was published under the journal’s contributor track, which allows a member of the National Academy of Sciences to submit two papers per year. Crucially, the preferential process allows the submitter to choose the reviewers who will evaluate the study. That’s unlike a typical paper in the journal, where the journal selects the reviewers. In this case, both the authors and the reviewers of the study were not epidemiologists, as might be expected for a paper on this topic, but scientists who study aerosols.

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The referenced PNAS paper (published June 11, 2020):

“Identifying airborne transmission as the dominant route for the spread of COV-19”

[Raven-Knightly]

(Scientific American, June 22, 2020):

“The Risks of Rushing a COVID-19 Vaccine -
Telescoping testing time lines and approvals
may expose all of us to unnecessary dangers”

The excitement and enthusiasm for a COVID-19 vaccine by the end of 2020 is both palpable and understandable. We all hope for a rapid end to the pandemic and an effective vaccine would be a surefire solution. But there are risks that come with a fast-tracked vaccine delivered end of this year, not the least of which are the risks related to the safety of the vaccine itself.

Telescoping testing timelines and approvals may expose all of us to unnecessary dangers related to the vaccine. … The US alone plans to vaccinate hundreds of millions of people with the first successful candidate. One serious adverse event per thousand of a vaccine given to 100 million people means harm to 100,000 otherwise healthy people.

Aside from questions of safety that attend any vaccine, there are good reasons to be especially cautious for COVID-19. Some vaccines worsen the consequences of infection rather than protect, a phenomenon called antibody-dependent enhancement (ADE). ADE has been observed in previous attempts to develop coronavirus vaccines. To add to the concern, antibodies typical of ADE are present in the blood of some COVID-19 patients. Such concerns are real. … Questions also arise around the efficacy of a potential vaccine. The little we know of the current generation of COVID-19 vaccines raises serious questions regarding their ability to protect people from infection. …

… at least some of the candidate vaccines did raise significant immune responses. How that translates to protection of humans is uncertain though as monkeys do not become noticeably ill or exhibit many of the life-threatening consequences of COVID-19, even when exposed to high doses of the virus via the nose, lung, and rectum simultaneously. As many of the most serious COVID symptoms do not appear until late in the disease course, sometimes four to five weeks following exposure, there is a possibility that we will not have sufficient time to judge efficacy of a new vaccine, even by the lower standard of symptom amelioration.

An effective COVID-19 vaccine also faces several hurdles beyond our control. The older we get the poorer our ability to respond to vaccines. Resistance to vaccination begins early at age 30 and becomes progressively more profound with time. That is especially troubling as those over 60 are the population most at risk. Vaccination of the elderly may sometimes succeed by administering repeated doses and by increasing the potency of the vaccine with powerful adjuvants. But these adjuvants can be especially risky for the very old. …

… There is no doubt we need an urgent end to the pandemic. Economies around the world are crashing. Governments are piling up trillions of dollars in debt. And, in the US alone, tens of millions are without work or income. But there are still costs that are too great, even when compared to such numbers. When we have solutions to the pandemic in hand we cannot risk the potential lives lost of rushing a COVID vaccine to market.

[Raven-Knightly]

(The Atlantic, June 30, 2020):

“A Dire Warning From COVID-19 Test Providers -
U.S. coronavirus testing could fail again,
as surging demand creates new backlogs and delays.”

The United States is once again at risk of outstripping its COVID-19 testing capacity, an ominous development that would deny the country a crucial tool to understand its pandemic in real time.

The American testing supply chain is stretched to the limit, and the ongoing outbreak in the South and West could overwhelm it, according to epidemiologists and testing-company executives. While the country’s laboratories have added tremendous capacity in the past few months- the U.S. now tests about 550,000 people each day, a fivefold increase from early April - demand for viral tests is again outpacing supply.

If demand continues to accelerate and shortages are not resolved, then turnaround times for test results will rise, tests will effectively be rationed, and the number of infections that are never counted in official statistics will grow. Any plan to contain the virus will depend on fast and accurate testing, which can identify newly infectious people before they set off new outbreaks. Without it, the U.S. is in the dark. …

… In mid-June, four changes hit all at once, Cohen said. Large companies began to test their employees en masse, hospitals started to test every patient who needed an elective procedure, and nursing homes started regularly testing their employees and some residents. The American public also seemed to seek out voluntary tests in greater numbers this month. …

… The American Clinical Laboratory Association, a trade group that represents testing labs, has … warned of shortages. “While our members are collectively performing hundreds of thousands of tests each day, the anticipated demand for COVID-19 testing over the coming weeks will likely exceed members’ testing capacities,” said Julie Khani, its president, in a statement. The group’s members conduct about half of the country’s daily coronavirus tests, according to information in her statement.

[Raven-Knightly]

(Gizmodo, July 1, 2020):

“4 Unusual Things We’ve Learned About Coronavirus
Since the Start of the Pandemic”

Many inflammatory diseases, including infections, are associated with an increased risk of developing blood clots. However, COVID-19 is more strongly associated with blood clots than many other infections.

If blood clots are large enough, they can block the flow of blood through a blood vessel. This in turn leads to the part of the body the blood vessel supplies being starved of oxygen. If this happens in a coronary artery, which supplies blood to your heart, it can cause a heart attack. In the lungs, it can cause a pulmonary embolism. In the brain, it can cause a stroke, which we have seen even in young people with COVID-19 but no other risk factors.

Critically ill COVID-19 patients in intensive care units (ICU) are particularly at risk of blood clots. One study found 49% of patients were affected, mainly with clots to the lungs. Other studies found 20-30% of critically ill COVID-19 patients had blood clots. These rates are much higher than we’d expect to see in patients admitted to ICU for other reasons. Worryingly, clots occur in COVID-19 patients despite using standard preventative measures such as blood-thinning drugs.

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(American Society of Hematology, Blood, June 23, 2020):

“Platelet Gene Expression and Function in COVID-19 Patients”

There is an urgent need to understand the pathogenesis of coronavirus disease 2019 (COVID-19). In particular, thrombotic complications in patients with COVID-19 are common and contribute to organ failure and mortality. Patients with severe COVID-19 present with hemostatic abnormalities that mimic disseminated intravascular coagulopathy associated with sepsis with the major difference being increased risk of thrombosis rather than bleeding. However, whether SARS-CoV-2 infection alters platelet function to contribute to the pathophysiology of COVID-19 remains unknown. In this study, we report altered platelet gene expression and functional responses in patients infected with SARS-CoV-2. …

… COVID-19 is most commonly associated with acute respiratory distress syndrome and hypoxemic respiratory failure. Significant derangements in the coagulation cascade have been observed in critically ill COVID-19 patients, including elevated D-dimers, fibrinogen and VWF levels. Furthermore, thrombosis, including pulmonary embolism, venous thrombosis, and ischemic stroke are common among severely ill patients. Platelets are known to play a significant role in the development of these thrombotic complications. In addition, platelets are an important bridge between the hemostatic system and immune defense, including viral illness. Whether COVID-19 alters platelet gene expression and function is unknown. We demonstrate for the first time that COVID-19 significantly alters platelet gene expression and triggers robust platelet hyper-reactivity.

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(Cell Journal pre-proof, June 18, 2020):

“Human iPSC-Derived Cardiomyocytes are Susceptible to SARS-CoV-2 Infection”

Coronavirus disease 2019 (COVID-19) is a pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is defined by respiratory symptoms, but cardiac complications including viral myocarditis are also prevalent. Although ischemic and inflammatory responses caused by COVID-19 can detrimentally affect cardiac function, the direct impact of SARS-CoV-2 infection on human cardiomyocytes is not well-understood. …

… Results presented here establish that human iPSC-derived cardiomyocytes are susceptible to ACE2-mediated direct infection by SARS-CoV-2, and that the virus may induce detrimental cytopathic effects in these cells.

[Raven-Knightly]

(Boston, June 30, 2020):

“Most people with coronavirus won’t spread it. Why do a few infect many? -
Growing evidence shows most infected people aren’t spreading the virus.
But whether you become a super-spreader
probably depends more on circumstance than biology.”

In a preprint published last week, the researchers found many superspreading events. Just 2% of people were responsible for 20% of transmissions. Now researchers are trying to figure out why so few people spread the virus to so many. They’re trying to answer three questions: Who are the superspreaders? When does superspreading take place? And where? …

A lot of transmission seems to happen in a narrow window of time starting a couple days after infection, even before symptoms emerge. If people aren’t around a lot of people during that window, they can’t pass it along.

… certain places seem to lend themselves to super-spreading. A busy bar, for example, is full of people talking loudly. Any one of them could spew out viruses without ever coughing. And without good ventilation, the viruses can linger in the air for hours. A study from Japan this month found clusters of coronavirus cases in health care facilities, nursing homes, day care centers, restaurants, bars, workplaces, and musical events such as live concerts and karaoke parties.

This pattern of super-spreading could explain the puzzling lag in Italy between the arrival of the virus and the rise of the epidemic. And geneticists have found a similar lag in other countries: The first viruses to crop up in a given region don’t give rise to the epidemics that come weeks later.

[Raven-Knightly]

(Seattle Times, June 30, 2020):

“Protests don’t appear to be driving coronavirus surge in Seattle area
or elsewhere, researchers say”

… some researchers say that the protests do not appear to be significantly driving this surge. This helps bolster the case that the coronavirus generally does not transmit as easily outdoors, where even a gentle breeze can help diffuse the virus, compared to confined indoor spaces. “I would say that outside makes a big difference because of much more air circulation,” said Dr. Jared Baeten, a vice dean at the University of Washington’s School of Public Health, who donned a mask and joined in the June 12 March of Silence through Seattle that drew an estimated 60,000 people.

In King County, the epicenter of Washington’s protests, health investigators have tracked - during a 19-day span in June - less than 5% of 1,008 total positive cases to people who attended protests. In other cities, including Minneapolis and Portland, researchers have yet to find that protests, where many were masked, have caused major spikes in cases. “The data may be imperfect but … neither here in King County, or elsewhere in the county, where health care authorities are looking, have we been able to document that or find strong evidence of that,” said Dr. Jeffrey Duchin, health officer of Public Health, Seattle & King County in remarks to reporters on Friday.

Others have reached a similar conclusion. A working paper - yet to be peer reviewed - from the National Bureau of Economic Research analyzed data from protests in 315 large cities and found “no evidence that urban protests reignited COVID-19 case growth during the more than three weeks following the protest.” The study also cited evidence that protests prompted more stay-at-home behavior by those who didn’t go to the protests.

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(Washington Post, June 30, 2020):

“Protests probably didn’t lead to coronavirus spikes,
but it’s hard to know for sure”

… some public health officials and disease trackers say there appears to be scant evidence the protests sparked widespread outbreaks. Others say that because many states reopened about the same time as the protests, and because of the limits of contact tracing, they simply can’t say for sure. … most experts say the protests are probably not to blame, or almost certainly not the only thing to blame in places where cases are soaring. …

… Absent a few positive tests among protesters announced here and there, the only major outbreak tied to protests happened in South Carolina, where organizers postponed demonstrations or moved them online after at least 13 people who took part in previous protests tested positive. … data from other cities suggests protests have not been followed by an increase in cases of covid-19, the disease caused by the novel coronavirus. Minneapolis, where Floyd was killed and where the protests began, has registered a steady decrease in case numbers this month. … Health systems in the area that tested thousands of people who attended the demonstrations returned positivity rates of less than 1 percent. … Officials in New York and Philadelphia … say they see no evidence of cases accumulating because of the protests. … In Seattle; Portland, Ore.; and Oakland, Calif. - cities experiencing a coronavirus resurgence - officials have asked people testing positive whether they attended protests, and few said they had. …

… The same is true in Seattle. Out of more than 1,000 positive tests in recent weeks, 34 of the people testing positive said they attended a protest or mass gathering since late May, according to King County Health Officer Jeff Duchin. Nearly 3,000 people who said they were at protests have been tested by the city, and fewer than 1 percent were positive, Duchin said. … In other places, the impact of the protests is less clear. Brent Andrew, spokesman for San Francisco’s Department of Public Health, said the city is still monitoring potential ties between a recent surge in cases and protests. In Houston, at the epicenter of a covid-19 crisis in Texas, officials attribute rising case loads to a variety of factors - and say protests could be one. …

… available data suggests the protests did not ignite the same kind of outbreaks associated with some conferences, choir practices and religious services. Many epidemiologists and virologists suggest being outside allows coronavirus-infected particles to disperse more easily, making outdoor gatherings - such as protests - less dangerous than those inside.

[Raven-Knightly]

(JAMA, July 1, 2020):

“Estimation of Excess Deaths Associated With the COVID-19 Pandemic
in the United States, March to May 2020”

Question: Did more all-cause deaths occur during the first months of the coronavirus disease 2019 (COVID-19) pandemic in the United States compared with the same months during previous years?

Findings: In this cohort study, the number of deaths due to any cause increased by approximately 122 000 from March 1 to May 30, 2020, which is 28% higher than the reported number of COVID-19 deaths.

Meaning: Official tallies of deaths due to COVID-19 underestimate the full increase in deaths associated with the pandemic in many states. …

… Results: There were approximately 781 000 total deaths in the United States from March 1 to May 30, 2020, representing 122 300 (95% prediction interval, 116 800-127 000) more deaths than would typically be expected at that time of year. There were 95 235 reported deaths officially attributed to COVID-19 from March 1 to May 30, 2020. The number of excess all-cause deaths was 28% higher than the official tally of COVID-19–reported deaths during that period. In several states, these deaths occurred before increases in the availability of COVID-19 diagnostic tests and were not counted in official COVID-19 death records. There was substantial variability between states in the difference between official COVID-19 deaths and the estimated burden of excess deaths.

Conclusions and Relevance: Excess deaths provide an estimate of the full COVID-19 burden and indicate that official tallies likely undercount deaths due to the virus. The mortality burden and the completeness of the tallies vary markedly between states. …

Discussion: … The gap between reported COVID-19 deaths and excess deaths can be influenced by several factors, including the intensity of testing; guidelines on the recording of deaths that are suspected to be related to COVID-19 but do not have a laboratory confirmation; and the location of death (eg, hospital, nursing home, or unattended death at home). For instance, deaths that occur in nursing homes might be more likely to be recognized as part of an epidemic and correctly recorded as due to COVID-19. As the pandemic has progressed, official statistics have become better aligned with excess mortality estimates, perhaps due to enhanced testing and increased recognition of the clinical features of COVID-19. In New York City, official COVID-19 death counts were revised after careful inspection of death certificates, adding an extra 5048 probable deaths to the 13 831 laboratory-confirmed deaths. 19 As a result, the all-cause excess mortality burden from March 11 to May 2, 2020, is only 27% higher than official COVID-19 statistics. 19 This aligns well with our estimate of 26% for a similar period in New York City, using a slightly different modeling approach.

Many European countries have experienced sharp increases in all-cause deaths associated with the pandemic. Real-time all-cause mortality data from the EuroMomo project (https://www.euromomo.eu/) demonstrate gaps between the official COVID-19 death toll and excess deaths that echo findings in our study. These gaps are more pronounced in countries that were affected more and earlier by the pandemic and had weak testing. Very limited excess mortality information is available from Asia, Africa, the Middle East, and South America thus far; these data will be important to fully capture the heterogeneity of death rates related to the COVID-19 pandemic across the world. Prior work on the 1918 and 2009 pandemics has shown substantial heterogeneity in mortality burden between countries, in part related to health care. 8, 20

[Raven-Knightly]

(Washington Post, July 1, 2020):

“Coronavirus autopsies: A story of 38 brains, 87 lungs and 42 hearts -
What we’ve learned from the dead that could help the living.”

Among the most important findings, consistent across several studies, is confirmation the virus appears to attack the lungs the most ferociously. They also found the pathogen in parts of the brain, kidneys, liver, gastrointestinal tract and spleen and in the endothelial cells that line blood vessels, as some had previously suspected. Researchers also found widespread clotting in many organs. …

… Given widespread reports about neurological symptoms related to the coronavirus, Fowkes said, she expected to find virus or inflammation - or both - in the brain. But there was very little. When it comes to the heart, many physicians warned for months about a cardiac complication they suspected was myocarditis, an inflammation or hardening of the heart muscle walls - but autopsy investigators were stunned that they could find no evidence of the condition. Another unexpected finding, pathologists said, is that oxygen deprivation of the brain and the formation of blood clots may start early in the disease process. That could have major implications for how people with covid-19 are treated at home, even if they never need to be hospitalized. …

… One of the first American investigations to be made public, on April 10, was out of New Orleans. The patient was a 44-year-old man who had been treated at LSU Health. Richard Vander Heide remembers cutting the lung and discovering what were probably hundreds or thousands of microclots. … as he moved onto the next patient and the next, Vander Heide saw the same pattern. He was so alarmed, he said, that he shared the paper online before submitting it to a journal so the information could be used immediately by doctors. The findings caused a stir at many hospitals and influenced some doctors to start giving blood thinners to all covid-19 patients. It is now common practice. The final, peer-reviewed version involving 10 patients was subsequently published in the Lancet in May. Other lung autopsies - including those described in papers from Italy of 38 patients, a Mount Sinai Health study on 25 patients, a collaboration between Harvard Medical School and German researchers on seven and an NYU Langone Health study on seven - have reported similar findings of clotting. Most recently, a study out last month in the Lancet’s eClinicalMedicine, found abnormal clotting in the heart, kidney and liver, as well as the lungs of seven patients, leading the authors to suggest this may be a major cause of the multiple-organ failure in covid-19 patients.

[Raven-Knightly]

(Cornell University College of Life Sciences, Alliance for Science, June 30, 2020):

“What are the Top 5 most promising COVID-19 vaccine candidates?”

As we recently told Reuters in an interview, “No, DNA vaccines will not lead to genetically engineered humans.” However, the technique does involve injecting a fragment of circular DNA, called a plasmid, into human cells. This introduced DNA codes for SARS-CoV-2 viral proteins that are then expressed by the cell and help prime the immune system to fight off an attack by COVID-19. Like mRNA, this is a new technology - no DNA vaccines have ever been fully developed and utilized in humans to prevent disease.

[SessionDrummer]

@Mikser

CUHREEPY

[Raven-Knightly]

(Washington Post, July 1, 2020):

“Lawmakers call for more transparency in health agency’s pandemic data collection practices -
HHS, which reports to the White House, will use technology company Palantir to analyze the data”

A growing number of Democratic lawmakers are sounding the alarm about a program launched by the U.S. Department of Health and Human Services to track the spread of the coronavirus. The public health effort, dubbed “HHS Protect Now,” hoovers up vast amounts of data, including coronavirus test results, from the Centers for Disease Control and Prevention, as well as state and local sources. It also relies on technology from secretive Silicon Valley firm Palantir, better known for working with the U.S. military, national security agencies, immigration offices.

In a letter shared with The Washington Post and sent Tuesday evening to HHS Secretary Alex Azar, a group of Democratic U.S. senators and members of Congress, including Sen. Elizabeth Warren (D-Mass.) and Richard Blumenthal (D-Conn.), called for more transparency around the initiative. The letter questioned whether any of the data gathered would be shared with U.S. Immigration and Customs Enforcement to round up undocumented immigrants. “We are concerned that, without any safeguards, data in HHS Protect could be used by other federal agencies in unexpected, unregulated, and potentially harmful ways”.

[Raven-Knightly]

@Mikser

Here is the inconvenient truth about DNA vaccines.
They will permanently alter your DNA.

“Still, Dr. Baltimore says" - (Note: in 2015) - "that he envisions that some people might be leery of a vaccination strategy that means altering their own DNA, even if it prevents a potentially fatal disease.” … I don’t hold up the scientific work of any of these men for great acclaim. I’m only interested in which man knows whether a DNA vaccine would permanently alter the genetic makeup of every recipient’s DNA. David Baltimore is a Nobel Laureate (1975, in Physiology/Medicine), and the past president of the American Association for the Advancement of Science (1997-2006). He’s one of the most famous scientists in the world.

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Click here to see article author Jon Rappoport information at SourceWatch

Now that InfoWars contributor Jon R. has definitively solved this most complicated puzzle surrounding Vaccinology, I shall surely look forward to reading his wisdoms surrounding magic, past life regression, and development of paranormal abilities.

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(Recent Patents on Anti-cancer Drug Discovery, January, 2014):

“Recent Advances in Design of Immunogenic and Effective
Naked DNA Vaccines Against Cancer”

A variety of clinical trials for vaccines against cancer have provided evidence that DNA vaccines are well tolerated and have an excellent safety profile.

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(International Journal of Molecular Science, November 15, 2018):

“DNA Vaccines - How Far From Clinical Use?”

The use of DNA vaccines has early raised safety concerns mainly concerning the probability of stable integration of transfected DNA into the genome of somatic or even germ cells, causing dysregulated gene expression and mutations. … safety concerns of DNA vaccines need to be considered with regard to their translational use in the clinic [32]. … Presently, there are no approved DNA vaccines for use in humans. Nevertheless, some DNA-based vaccines were approved by the FDA and the USDA for veterinary use. … The overall safety of DNA vaccines has been thoroughly proven in several clinical trials, underlined by the fact that no antibody response against prokaryotic parts of the DNA vaccine itself has been observed and that adverse effects are limited to mild local reactivity at the injection site [2].

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(The Lancet, July 24, 2019):

“Safety and immunogenicity
of an anti-Middle East respiratory syndrome coronavirus DNA vaccine:
a phase 1, open-label, single-arm, dose-escalation trial”

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(Philadelphia Enquirer, June 26, 2020):

“Coronavirus could be turning point for a vaccine technology 30 yrs in the making”

(Philadelphia Enquirer, June 30, 2020):

“Inovio’s coronavirus vaccine shows promise in early testing, but details are few”

(Genetic Engineering and Biotechnology News, June 30, 2020):

“INOVIO Reports Positive Interim Phase I Data for COVID-19 DNA Vaccine,
Joins “Warp Speed” Primate Study”

[Raven-Knightly]

By the way, DNA Vaccination and CRISPR genome editing are two different things.

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(STAT, February 19, 2019):

“Vaccines don’t work against some viruses. CRISPR might one day fix that”

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(WIRED, March 18, 2020):

“Could Crispr Be Humanity’s Next Virus Killer? -
Stanford scientists are exploring whether gene-editing technology can be used to fight pandemics. But so far, they have just one piece of a larger puzzle.”

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(NIH Nat. Library of Medicine): “What are genome editing and CRISPR-Cas9?”

[Raven-Knightly]

(BMJ, July 1, 2020):

“Diagnostic accuracy of serological tests for covid-19:
systematic review and meta-analysis”

In this systematic review and meta-analysis, existing evidence on the diagnostic accuracy of serological tests for covid-19 was found to be characterised by high risks of bias, heterogeneity, and limited generalisability to point-of-care testing and to outpatient populations. We found sensitivities were consistently lower with the LFIA method compared with ELISA and CLIA methods. For each test method, the type of immunoglobulin being measured - IgM, IgG, or both - was not associated with diagnostic accuracy. Pooled sensitivities were lower with commercial kits and in the first and second week after symptom onset compared with the third week or later. Pooled specificities of each test method were high. However, stratified results suggested specificity was lower in individuals with suspected covid-19, and that other viral infections could lead to false positive results for the LFIA method. These observations indicate important weaknesses in the evidence on covid-19 serological tests, particularly those being marketed as point-of-care tests. …

… the poor performance of existing serological tests for covid-19 raises questions about the utility of using such methods for medical decision making, particularly given time and effort required to do these tests and the challenging workloads many clinics are facing. Our findings should also give pause to governments that are contemplating the use of serological tests - in particular, point-of-care tests - to issue immunity “certificates” or “passports.” For example, if an LFIA is applied to a population with a true SARS-CoV-2 prevalence of 10%, for every 1000 people tested, 31 who never had covid-19 will be incorrectly told they are immune, and 34 people who had covid-19 will be incorrectly told that they were never infected.

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So-called “pooled” testing is when numerous individual samples are combined into one - in order to conserve supplies of testing materials. If a “pooled” sample returns a “negative” result, then all the individuals “pooled” are assumed to be “negative”.

[Raven-Knightly]

(Karolinska Institutet, June 30, 2020):

“Immunity to COVID-19 is probably higher than tests have shown”

New research from Karolinska Institutet and Karolinska University Hospital shows that many people with mild or asymptomatic COVID-19 demonstrate so-called T-cell-mediated immunity to the new coronavirus, even if they have not tested positively for antibodies. According to the researchers, this means that public immunity is probably higher than antibody tests suggest. …

… “T cells are a type of white blood cells that are specialised in recognising virus-infected cells, and are an essential part of the immune system,” says Marcus Buggert, assistant professor at the Center for Infectious Medicine, Karolinska Institutet, and one of the paper’s main authors. “Advanced analyses have now enabled us to map in detail the T-cell response during and after a COVID-19 infection. Our results indicate that roughly twice as many people have developed T-cell immunity compared with those who we can detect antibodies in.” …

… “One interesting observation was that it wasn’t just individuals with verified COVID-19 who showed T-cell immunity but also many of their exposed asymptomatic family members,” says Soo Aleman. “Moreover, roughly 30 per cent of the blood donors who’d given blood in May 2020 had COVID-19-specific T cells, a figure that’s much higher than previous antibody tests have shown.”

The T-cell response was consistent with measurements taken after vaccination with approved vaccines for other viruses. Patients with severe COVID-19 often developed a strong T-cell response and an antibody response; in those with milder symptoms it was not always possible to detect an antibody response, but despite this many still showed a marked T-cell response. …

… T-cell analyses are more complicated to perform than antibody tests and at present are therefore only done in specialised laboratories, such as that at the Center for Infectious Medicine at Karolinska Institutet. “Larger and more longitudinal studies must now be done on both T cells and antibodies to understand how long-lasting the immunity is and how these different components of COVID-19 immunity are related,” says Marcus Buggert. The results are so new that they have not yet undergone peer review ahead of publication in a scientific journal. Pending such review, the article has been published as preprint on bioRxiv.

[anon84779643]

[daath]

Just took my oldest daughter to do an antibody test - it was positive - took one myself, hoping for a positive, but alas, it was negative