A short addendum to my pre-print on early Wuhan #SARSCoV2 sequences deleted from the Sequence Read Archive (), courtesy of an anonymous Twitter user. (1/n)
It turns out that mention of the sequencing project in question (PRJNA612766) also disappeared from China National GeneBank (CNGB) shortly after it was removed from the NIH Sequence Read Archive. (2/n)
On June-19-2020: web.archive.org/web/2020061904… (3/n) Image
On July-3-2020: web.archive.org/web/2020070306… (4/n) Image

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More from @jbloom_lab

24 Jun
I am getting lots of questions if my pre-print about some #SARSCoV2 sequences that were removed from Sequence Read Archive tell us anything about lab accident versus natural zoonosis.

I posted summary of pre-print below, but did not directly address this point explicitly (1/n)
The answer is NO. The people using it to strongly support either argument are those that have become so emotionally invested in their opinion that they have lost the ability to analyze anything objectively outside of the framework of that argument. (2/n)
What the pre-print does imply is as follows:

First, there may be additional relevant data in obscure locations that aren't the places where we are accustomed to looking (e.g., on the Google Cloud, in table 1 of a paper on diagnostics, etc): (3/n)
Read 5 tweets
22 Jun
In a new study, I identify and recover a deleted set of #SARSCoV2 sequences that provide additional information about viruses from the early Wuhan outbreak: biorxiv.org/content/10.110… (1/n)
Specifically, NIH maintains the Sequence Read Archive, where scientists around world deposit deep sequencing data for others to analyze. I noted peerj.com/articles/9255 lists all #SARSCoV2 data in archive as of March-31-2020. Most from a project by Wuhan University. (2/n)
But when I went to Sequence Read Archive, I found entire project was gone! (Note that as detailed below, this does *not* imply malfeasance by NIH. Sequence Read Archive policy allows submitters to delete by e-mail request.) (3/n)
Read 26 tweets
29 May
In a new study led by the group of Hui-Ling Yen, we help define the transmission potential of flu viruses replicating in the upper and lower respiratory tract, and quantify the rate of mixing between viruses in these two locations: academic.oup.com/jid/advance-ar… (1/n)
Specifically, our results show that at least in ferrets, viruses transmit from the upper rather than lower respiratory tract, and there is only limited slow mixing between viral populations in these two anatomical locations. (2/n)
Specifically, we generated pdmH1N1 viruses that were either "wildtype" or had 2 synonymous mutations that served as neutral genetic markers. Ferrets were then inoculated with one of these viral variants in the upper airway, and one in the lower airway. (3/n)
Read 5 tweets
13 May
In letter published in @ScienceMagazine today, I join 17 other scientists in calling for further investigation of #SARSCoV2 origins, including objective consideration of both accidental lab leak and natural zoonosis: science.sciencemag.org/lookup/doi/10.… (1/n)
We note the scientific community has made admirable progress in understanding biology of #SARSCoV2, including developing vaccines & other countermeasures. But more investigation needed to determine origin of pandemic, which is critical to mitigating risk of future outbreaks (3/n)
Read 11 tweets
23 Apr
We've written a perspective on a new study by @MAMdayIndayOut that helps explain why some viruses (measles) don't evolve to escape immunity but others (influenza) do. Provides some clues relevant to future for #SARSCoV2 as well: cell.com/cell-reports-m…

Here is a recap: (1/n)
Measles and influenza are both respiratory RNA viruses with high mutation rates. Immunity to measles is lifelong: before vaccines, people were infected just once in their lives. Then a measles vaccine was developed >50 years ago and it still works great today. (2/n)
Unfortunately, same is not true for influenza. Typical person is re-infected with same subtype of influenza every 5-7 yrs. Importantly, influenza re-infections are *not* because immunity is weak or transient. We know this from the 1977 flu pandemic. (3/n)
Read 20 tweets
14 Apr
In new study, we compared specificity of #SARSCoV2 antibody response elicited by Moderna mRNA-1273 vaccine vs infection. Some interesting differences: vaccine neut activity more RBD targeted, but has broader binding within RBD: biorxiv.org/content/10.110… (1/n)
First @AllieGreaney & Andrea Loes quantified how important RBD-binding antibodies were for neutralization by mRNA-vaccine- and infection-elicited sera. Vaccine sera neutralization was highly RBD directed: >90% of neut by nearly all vaccine sera due to RBD-binding antibodies (2/n) Image
This result is interesting, as mRNA-1273 encodes entire spike ectodomain with stabilizing 2P mutations. But either those mutations or differences in antigen presentation by mRNA vaccine vs viral infection cause vaccine neut antibodies to focus more heavily on RBD. (3/n)
Read 14 tweets

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