Thread by @DrEricDing

Immunocompromised 45 year old suffered from #COVID19 for 155 days before he died. The virus was changing very quickly inside the man's body—it acquired a big cluster of >20 mutations—resembled the same ones seen in #B117 & #B1351. (NPR audio Part 1 of 2)🧵
npr.org/sections/goats…

2) NPR report audio part 2 of 2:

Dr. Li couldn't believe what they found. "I was shocked," he says. "When I saw the virus sequences, I knew that we were dealing with something completely different and potentially very important."

3) “Toward the very end of his life, he was treated with monoclonal antibodies, from Regeneron," Li says. "And shortly thereafter, we saw evidence that suggested the virus was developing resistance or escaping from these antibodies as well."

4) “Li and his colleagues published their findings in The New England Journal of Medicine in early November 2020 with little fanfare. Then about a month later, the pandemic took a surprising turn — and this peculiar case in Boston took on a new importance.

5) Scientists in the U.K. and South Africa announced they had detected new variants of the coronavirus. These variants were causing huge surges of COVID-19 in these countries.
When researchers looked at the genes of these variants, guess what they found?

6) A cluster of mutations that looked remarkably similar to the mutations found in the virus from the Boston patient. The sets of mutations weren't exactly identical, but they shared important characteristics...

7) They both had about 20 mutations, and they shared several key ones, including a mutation (N501Y) known to help the virus bind more tightly to human cells and another mutation (E484K) known to help the virus evade antibody detection.

8) So we have a number of examples, around the planet, in which patients' viruses suddenly have a whole mess of new mutations all at once," says virologist Jeremy Luban at the University of Massachusetts Medical School. And other cases have likely gone undetected, he says.

9) So scientists are starting to think the two phenomena could be related. That perhaps new variants arose inside people similar to the man in Boston —that is, people who are immunocompromised & have long-term #COVID19 infections.
"I think that's the leading theory," Luban says.

10) long-term infections are mutational testing ground. While inside 1 person, the virus can try out many different combinations of mutations and figure out, through trial and error, which ones are best at evading the immune system or helping the virus become more infectious.

11) My take: the moral lesson is that, when given time and opportunity, the virus finds a way. The virus is a cunning mutating beast that will try every way to defeat us if we let it keep proliferating. We must stop it FAST, or else it will even our countermeasures. Like this:

https://twitter.com/drericding/status/1358830506549379082

12) And the virus will even evade people who has had prior immunity and prior antibodies to the older common #SARSCoV2. Such as this example — here not even people were protected from severe disease even if with prior immunity.

https://twitter.com/drericding/status/1358065355785134083

13) here the the NEJM on the 45 year old immunocompromised patient who was sick for 155 days straight before he died. Poor guy. nejm.org/doi/full/10.10…

14) and now we have a looming surge in the US with the #B117 variant. All because we let this virus out of control.

https://twitter.com/drericding/status/1358468446548357123

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