IVM’s 80% efficacy vs. vaccine 95% efficacy means that 5 TIMES more people would get sick using IVM for prophylaxis than vaccinated people in the same period.
Also, those 80% and 95% are not identical, as the time periods in which vaccines were evaluated are MUCH longer.
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Most IVM trials lasted a few weeks while the vaccine trials lasted for months.
Also, if you look at the vaccine efficacy graph above, you will see that after the first 14 days when most of the infections in the vax group happen, the vax curve remains almost flat!
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Which means that after the initial 14 days after the jab — which is the time it takes for your immune system to start generating adequate protection — the protection offered by a vaccine is closer to 99% levels.
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This is corroborated by follow up data on breakthrough infections: fewer than 0.1% of vaccinated people have ever developed COVID in the follow up period. These are amazing numbers.
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And those breakthrough cases are milder than cases in unvaccinated people:
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Finally, to get any prophylactic protection from IVM you would have to take it continuously for months. And weekly dosage is too infrequent as its half-life is 18 hours, so after 3.5 days you only have 1/32 of the initial dose left in your body.
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So @Daoyu15 pointed to this great preprint that once again confirmed that RaTG13 doesn't bind well to bat ACE2. The beauty of this work is that it tested ACE2 of the very species RaTG13 was allegedly sampled from, R. affinis.
As this figure shows, RaTG13 is really bad at binding to R. affinis bat ACE2. Even the T403R mutation that makes it bind really well to human ACE2 is helpless when it comes to R. affinis ACE2. Weird? Weird.
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What is even more weird is how well it binds to human ACE2. Sure it's no champ like SARS2 but RaTG13 binds to human ACE2 just 1/2 as well (100k cells/well), which is also about 8x better than SARS2 does to R. affinis ACE2 (12k cells/well) (see above fig.)
Another rabbit hole on the topic of SARS2 as a potential pan-coronavirus vaccine candidate. This time it was prompted by @gdemaneuf pointing out several papers that say SARS2 spike might bind not just to ACE2 but also to the MERS receptor, DPP4.
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There have been several papers just after the outbreak of SARS2 that hypothesized that it could also invade immune system cells via DPP4 receptor, mostly based on in silico modeling. Then a couple papers reported that in actual experiments it doesn’t and this topic died down
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But even if it doesn’t bind to the MERS receptor, the presence of those residues in its spike is intriguing, as they could come from someone trying to make it bind and/or trying to generate neutralizing antibodies against those key residues with a goal of neutralizing MERS.
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Just so that we’re clear — I am not saying we should dismiss any COVID vaccine concerns. Absolutely not! We should debate any potential issues and closely monitor any actual ones. So far there do seem some rare minor issues and ultra-rare major ones (deaths, clots).
1/5
Not all vaccines are equal. Some are better than others. I am a huge fan of mRNA ones, I fully admit. I’ve been a fan of mRNA technology for many years (back when it was just invented/considered for use in Yamanaka factors delivery which are my main passion).
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Vaccines seem like a perfect fit for the mRNA technology, especially in a pandemic where you need very quickly adapt to novel strains. I actually hope we can squeak by without new boosters, but for that we need a coordinated world-wide effort to eradicate SARS2 ASAP.
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So some COVID vaccine alarmist have been quoting the study by @manorlaboratory out of Salk that SARS2 spike alone can cause cell damage. But that’s not what the study has shown!
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Those were not lone spike proteins, those were HIV-like virions encoding SARS2 spike. I.e. entered the cells expressing ACE2 and once inside expressed their proteins and maybe even integrated into cell genome (not sure if they used integrase-deficient retroviruses or not).
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Maybe the confusion is due to the lax wording by the popular science article describing the study: