1/7

Ok let’s try to estimate our annual risk of contracting COVID. We have these nice CDC data from when there were just 15M cases in the US (after about 6 months of the pandemic). Now it’s 33M, icymi.
2/7

Let’s look at the 40-64 age group. We have 5M cases out of ~100M ppl, i.e. a 5% incidence in 6 mo/15M cases, which I think we can extrapolate to 10M cases out of 30M/12mo. => annual risk of 10% for people aged 40-64.

Quick sanity check: 33M cases out of 330M is also 10%.
3/7

Now, what is the risk of death for people aged 40-64 who got COVID? Well, we got about 0.1M dead out of about 10M infected, which means a nice round CFR of 1%.
4/7

Putting the 2 numbers together, if you are 40-64 in the US, your chances of getting COVID and dying from it are 1 in 10*100 or 0.1%.

Or at least they would be if nobody was vaccinating. Fortunately, thanks to all people who got a jab, rates of new inf are rapidly dropping!
5/7

However, the chance to catch COVID and die is still quite sizable. Probably not 0.1% anymore, but even if it is 5-10x lower now thanks to vaccinations, it is still 0.01-0.02% for the unvaccinated.
6/7

How does that compare to your chances of dying from a jab?

Well, to date there’s been only 4434 *potential* deaths in the vaxxed, out of which only a few have been confirmed.

But even if ALL 4434 were caused by vaccines, that is still a negligible ~0.0044M/150M= 0.003%.
7/7

Which means that even in worst case vaccine scenario and best case reduced Covid transmission rates scenario, today your risk of getting Covid and dying is still 10-20x times higher (0.01-0.02%, up to 0.1%) than the risk of dying from a vaccine (<0.003%).

So go get a shot!

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More from @ydeigin

10 Apr
1/n

Ok, let me try and harp on my evolutionary, well, harp 😂 And maybe my favorite EvoBio couple, @HeatherEHeying and @BretWeinstein can smack me on the head if say something dumb.

So basically infectivity and virulence/pathogenicity are two different properties of a virus,
2/n

which *might* be correlated but do not have to be. First of all, we must understand: these little viruses are not out to kill us. All they “want” is to replicate. And want is in quotes because of course they don’t have any agency:
3/n

they are just a self-replicating collection of molecules, set in motion by some random LUCA prime mover billions of years ago. So the pathogenicity/virulence of a virus is really an unwanted side-effect for both parties:
Read 11 tweets
19 Mar
1/6 All right, today I got conclusive proof that Eddie Holmes sucks at aligning genomes. And if that’s not enough, I found the last nail in his “PAA insertion” coffin.

But first things first: he is a coauthor of a recent preprint with the following gem of an alignment (yellow):
2/6

See him putting the R in Rc-o319 alignment one aa ahead of others? That should immediately trigger a WTF moment in anyone even modestly familiar with genome alignments. Next, that urge should translate into checking the underlying nucleotides, which will quickly
3/6

confirm that the RSAN shouldn’t be shifted in Rc-o319 compared to its relatives but should neatly align with RSVN just above it, because it is the N in Rc-o319 that got duplicated (duplicate codons AAC AAC are a dead giveaway) — see my alignment above.

Embarrassing!!! 😂
Read 6 tweets
5 Mar
1/12

Ok, here goes nothing. Remember this little thing called a furin cleavage site? You know, the one that made SARS2 into a real promiscuous little virus? Well, as some have pointed out before, the strategy of inserting a furin cleavage site was not only
2/12

investigated by coronavirologists previously as a tool to expand virus tropism, but also by other virologists as a tool to actually ATTENUATE a virus. In other words, a vaccine strategy.

Getting goosebumps yet? I am.
3/12

So how could this be a vaccine strategy? Well, the idea, as I understand it, was to take a virus, insert some FCSs into it in key places, but do so in a cell culture that do NOT normally have furin, and thus the virus won’t get cut in such cells. But then if you infect
Read 13 tweets
22 Jan
Ok, the prize for the craziest and most dangerous gain-of-function research goes out to Italian virologists who took SARS2 and passaged it in vitro in the presence of neutralizing antibodies. It quickly obliged and mutated to escape them. Yay for a novel, more dangerous SARS3! 🤦‍♂️
Oh, and it developed a glycan sequon in vitro — take that, @K_G_Andersen! 😁 Image
Here’s the preprint:

biorxiv.org/content/10.110…
Read 4 tweets
22 Nov 20
Ok, does this conclusively disprove the PAA "insertion" in RmYN02? I re-ran the CLUSTAL W alignment with ALL genomes used in Zhou et al. (middle block below) and it shows NO trace of an insertion in RmYN02. I get the same result if I omit SARS2 from query (bottom block). 1/4
Here is the original figure from Zhou et al. claiming a PAA insertion. Btw, I couldn't find their nucleotide alignment in the paper, even in the Supplementary.

@CellCellPress @CurrentBiology could you please ask the authors to provide those data? 2/4
Here is the link to the paper: cell.com/current-biolog… 3/4
Read 6 tweets
28 May 20
1/n Here’s what still irks me in the EcoHealth/WIV narrative about RaTG13/4991. So in 2011 and 2012 Shi Zhengli goes on 2 expeditions to a bat cave near Kunming, the capital of Yunnan. There she finds CoV strains RsSHC014 and Rs3367 which share 85% and 96% with the first SARS-CoV
2/n This discovery is worthy of a Nature paper in 2013 and many subsequent accolades to its authors. Btw the first author of the 2013 Nature paper is Ge Xingyi, whose name features prominently on many other joint CoV papers. The team then proceeds to extract a live sample of
3/n Rs3367 which they then christen “WIV1” and later use as a backbone for several chimeric constructs. But for their 2015 joint chimera with Baric they used RsSHC014 as a backbone (85% similar to SARS).
Read 7 tweets

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