Covid 1/20/21 | COVID 19 Information Page

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The worse case scenario for vaccines and even immunity from previous infection – variant shows immunity to antibodies from previous infection! Its time to just get healthy. – https://www.biorxiv.org/content/10.1101/2021.01.18.427166v1.full.pdf

“SARS-CoV-2 501Y.V2, a novel lineage of the coronavirus causing COVID-19, contains multiple mutations

within two immunodominant domains of the spike protein. Here we show that this lineage exhibits

complete escape from three classes of therapeutically relevant monoclonal antibodies. Furthermore

501Y.V2 shows substantial or complete escape from neutralizing antibodies in COVID-19 convalescent

plasma. These data highlight the prospect of reinfection with antigenically distinct variants and may

foreshadow reduced efficacy of current spike-based vaccines.”

“N501Y has been shown to increase affinity for the human ACE2 receptor, which together with the repeated and

independent evolution of 501Y containing lineages25,26,31, strongly argues for enhanced transmissibility of

these new variants. Here we show that the 501Y.V2 lineage, that contains nine spike mutations, and

rapidly emerged in South Africa during the second half of 2020, is largely resistant to neutralizing

antibodies elicited by infection with previously circulating lineages. This suggests that, despite the many

people who have already been infected with SARS-CoV-2 globally and are presumed to have accumulated

some level of immunity, new variants such as 501Y.V2 pose a significant re-infection risk.”

“the data herein suggest that

most individuals infected with previous SARS-CoV-2 lineages will have minimal or no detectable

neutralization activity against 501Y.V2. T”

“he speed and scope of 501Y.V2 mediated immune escape from pre-existing neutralizing

antibodies highlight the urgent requirement for rapidly adaptable vaccine design platforms, and the need

to identify less mutable viral targets for incorporation into future immunogens.”

An interesting article highlighting the fact the virus is not killing us – its our response to the virus and some of us our body response is fatal. – In this article they focus on rogue antibodies vs. the cytokine storms. https://www.nature.com/articles/d41586-021-00149-1

“Early in the pandemic, researchers suggested that some people have an overactive immune response to COVID infection. Immune-system signalling proteins called cytokines can ramp up to dangerous levels, leading to ‘cytokine storms’ and damage to the body’s own cells. Clinical trials have now shown that some drugs that broadly dampen immune activity seem to reduce death rates in critically ill people, if administered at the right time.

But scientists studying COVID are increasingly also highlighting the role of autoantibodies: rogue antibodies that attack either elements of the body’s immune defences or specific proteins in organs such as the heart. In contrast to cytokine storms, which tend to cause systemic, short-duration problems, autoantibodies are thought to result in targeted, longer-term damage, says immunologist Akiko Iwasaki, a colleague of Ring’s at Yale.”

“In late September, a group led by Jean-Laurent Casanova at the Rockefeller University in New York City reported that more than 10% of 987 individuals with severe COVID-19 had antibodies that attacked and blocked the action of type 1 interferon molecules, which normally help to bolster the immune response against foreign pathogens1. That was a striking proportion, the researchers say, because people’s antibody repertoires are normally very dissimilar, and noone in a control group for the study had these antibodies. The researchers also saw the antibodies in people before their COVID-19 infection, so Casanova thinks that some people could be genetically predisposed to produce them. And the autoantibodies were more common in men than women — a possible factor in why COVID seems to hit men harder.”

“Iwasaki, Ring and others screened 194 patients and hospital workers with varying severities of COVID for a wide range of autoantibodies. Their study, which was posted online in December and has not yet been peer reviewed, found a higher prevalence of autoantibodies against the immune system in infected individuals than in uninfected people3. They found autoantibodies that attacked B cells, as well as some that attacked interferon.

But this study also suggested that SARS-CoV-2 might cause the body to generate autoantibodies that attack its own tissues. Some of the infected individuals had autoantibodies against proteins in their blood vessels, heart and brain. This was particularly intriguing because many of the symptoms seen in the pandemic are linked to these organs. It’s unclear whether COVID-19 infection caused the body to start making these autoantibodies or whether infected people had them already. Iwasaki says they are hoping to study other cases to establish whether there is a causal link; that would require obtaining more blood samples from before people become infected.”

“The autoantibody theory might explain some of the delay in the onset of severe symptoms in COVID-19. If evoked by the cellular damage and inflammation stoked by viral infection, as Lee and others think, autoantibodies would take a couple of weeks to build up in the body. This, he says, could be why much of the damage to tissues such as the lungs appears so long after a person develops symptoms such as fever. In this way, autoimmunity might be the real culprit behind the deadly destruction that continues after the coronavirus has cleared. “Clinicians are thinking, ‘Oh, this virus is so deadly, we’ve got to get rid of the virus.’ But then when you talk to the pathologists, they’re like, ‘Yeah, so we’re seeing all this damage, but not seeing much virus,’” Lee says.”

“If an autoimmunity element exists either in predisposing people to COVID-19 or in the fallout from the infection, there might be treatment implications. Casanova says that in cases in which pre-existing autoimmunity against interferon might put people at greater risk of falling ill, then blood tests for autoantibodies, which are becoming more available in research laboratories and university hospitals, could help to identify them.

And if these people become infected with SARS-CoV-2, Casanova suggests, they could receive supplementation as early as is practical with interferon-β, which is not as prone to attack from the immune system as are other interferons. Last November, a preliminary study found that an inhaled form of interferon-β seemed to improve the clinical condition of people with COVID, prompting a larger trial of this therapy9.”

“Even before autoantibodies came into focus, the idea that a cytokine storm might be a culprit meant that studies were under way to see whether immunosuppressive steroids such as dexamethasone, or the arthritis drugs tocilizumab and sarilumab, could be used to calm immune systems set awry by COVID. The World Health Organization now “strongly recommends” the use of dexamethasone in severe cases, and the United Kingdom is using the arthritis drugs for people with severe COVID after a clinical trial on 7 January10 suggested that they cut death rates in patients in intensive care.”

Data back up now…US is coming down only 2.7K deaths still Germany UK Mexico and Brazil over 1K