Is this the first direct evidence for a lab leak origin of COVID19?
A new research has again fuelled the debate on the origin of SARS2. Was SARS2 originated as an infectious clone assembled in vitro? 1/
But, why is it important to know exactly the origin of SARS2?
To prevent future pandemics, it is critical that we understand whether SARS2 spilled over directly from animals to people, or indirectly in a laboratory accident. 2/
The genome of SARS2 contains a peculiar pattern of unique restriction endonuclease recognition sites allowing efficient dis- and re-assembly of the viral genome characteristic of synthetic viruses. 3/
Here, the researchers report the likelihood of observing such a pattern in coronaviruses with no history of bioengineering. They find that SARS2 is an anomaly, more likely a product of synthetic genome assembly than natural evolution. 4/
The restriction map of SARS2 is consistent with many previously reported synthetic coronavirus genomes, meets all the criteria required for an efficient reverse genetic system….5/
It differs from closest relatives by a significantly higher rate of synonymous mutations in these synthetic-looking recognitions sites, and has a synthetic fingerprint unlikely to have evolved from its close relatives. 6/
The researchers conclude a high likelihood that SARS2 may have originated as an infectious clone assembled in vitro. 7/
@BallouxFrancois : “These findings are not 'final and dispositive', but they can't be ignored either. To me, this is by far the strongest piece of evidence to date against a simple scenario of strict zoonotic origin for SARS-CoV-2.”
A population based comparative study in #Japan studied 99 834 543 vaccinated individuals aged 12 years & older who have received SARS2 vaccine to investigate the association between SARS2 vaccination and #myocarditis death. 1/
Following are the key conclusions of the study:
1-SARS2 vaccination was associated with higher risk of myocarditis death, not only in young adults but also in all age groups including the elderly. 2/
2-Considering healthy vaccinee effect, the risk may be 4 times or higher than the apparent risk of myocarditis death. Underreporting should also be considered. 3/
Now, the noted virologist, @florian_krammer respond to this controversial research. According to him the problem was not in the research, but they did not ask the NIH if they were allowed to do so. 1/
What point the researchers were trying to prove! To be clear, nature did basically the same experiment before. It was called XD—a recombinant virus in the human population that combined spike of Omicron with the remaining genome from Delta via recombination 2/
Image @PeacockFlu
XD, when put in mice did the same. Delta killed the mice, XD killed the mice, Omicron did not
Fortunately, the XD recombinant fizzled out under pressure of other subvariants! 3/ @PeacockFlu
Omicron’s subvariants exhibit reduced fusogenicity and increased endosomal entry pathway utilization compared to the ancestral D614G variant, the underlying mechanisms of which remain elusive. 1/
Now the researchers show that the C-terminal S1 mutations of the BA.1.1 subvariant, H655Y and T547K, critically govern the low fusogenicity of Omicron. Notably, H655Y also dictates the enhanced endosome entry pathway utilization. 2/
Mechanistically, T547K and H655Y likely stabilize the spike trimer conformation, as shown by increased molecular interactions in structural modeling as well as reduced S1 shedding. 3/
Another instance of ‘Gain of Function’ research! Researchers are still creating a super deadly SARS2 variant in their labs. And we are still debating (& ‘doubting’) the lab leak theory in context with SARS2 origin!! 1/
Experts at Boston University created the most deadly version of Covid known to man, which could escape!
Someone rightly cautioned, “All it takes is one lab accident, one person not following protocol, one person deciding to skip a step and oops, it’s out of the lab” 2/
Omicron variant (BA.1) is highly transmissible, even in fully vaccinated individuals, and causes attenuated disease compared with other major VOCs. The Omicron spike (S) protein, with an unusually large number of mutations, is considered the major driver of these phenotypes. 3/
Why are elderly people more vulnerable to Covid even after vaccine boosters?
A new study offers some explanations. 1/
Individuals 70 y/o or older who received a primary 2-dose schedule with AZD1222 and booster 3rd dose with mRNA vaccine achieved significantly lower neutralizing antibody responses against SARS2 spike compared to those younger than 70 2/
One month after the booster neither the concentration of serum binding anti spike IgG antibody, nor the frequency of spike-specific B cells showed differences by age grouping. 3/