Arijit Chakravarty Profile picture
Apr 3 8 tweets 2 min read Read on X
@hallinen_diane @pan_accindex I think if someone’s going to make a claim like “Covid doesn’t harm your immune system”, that’s a bold claim.

If they’re wrong, the consequences will be much more severe than the unnecessary concern that would result from a false alarm. (1/)
@hallinen_diane @pan_accindex The claim itself is contrarian, as it flies in the face of the established science. It’s beyond meaningful debate at this point that *some* cases of Covid -even mild ones- lead to depletion of immune system components for months (2/)
@hallinen_diane @pan_accindex The people who would have us believe that this is no cause for concern base their argument on the fact that it (a) only happens to some people, (b) only happens for a little while or (c) happens with other viruses as well. All three statements are true. And irrelevant here (3/)
@hallinen_diane @pan_accindex This is a disease that most people can expect to get multiple times in their lives (our modeling suggests 1-2x/yr, in the absence of precautions), cumulative damage is well documented for other organ systems. Some -very nonzero - fraction of infections is persistent as well (4/)
@hallinen_diane @pan_accindex There’s no evidence suggesting that some people are uniquely vulnerable to immune depletion while others aren’t. It’s a Russell’s teapot to make the claim, and those who make it should produce the evidence to support it (5/)
@hallinen_diane @pan_accindex If you get the disease once a year and your immune system spends 6 months recovering each time, you are functionally immunocompromised- on average- when you look at it across the entire year. (6/)
@hallinen_diane @pan_accindex Repeated infections cause cumulative damage & intrahost viral evolution during persistent infections leading to immune evasion is well documented. Those who make the claim that such intrahost evo during persistent infections is rare should produce evidence to support it. (7/)
@hallinen_diane @pan_accindex False analogies to other viruses have been used by minimizers to confuse the issue from the get-go. Covid is not HIV, the flu or a cold. It’s an unprecedented public health threat, and the claim that there is no cause for concern is speculative. (8/8)

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More from @arijitchakrav

Jan 18
1/ Powerful testimony by @zalaly today in the Senate Hearing on Long COVID.

He makes a lot of really great points- well worth a watch!

There is no treatment for Long COVID. Recovery rates are low. (🧵👇)
2/ "The best way to prevent Long COVID is to prevent COVID in the first place". He makes a compelling case that this is something that requires government action.

In the meantime, we still have some agency as individuals, too. Check out:

typingmonkeys.substack.com/p/you-dont-nee…
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3/ The fewer times you get COVID, the better. If you do get COVID though, all is not lost, you can still move to limit your downside risk.

@TRyanGregory and I lay out the steps in the blog post below: Image
Read 6 tweets
Jan 10
@sunsweptforest Exactly. The big-name journals have a huge optimism bias.

In 2020&21, we predicted the virus would quickly evolve to evade immunity, that vaccines alone wouldn’t bring the pandemic to an end, that schools would seed disease, that appeals to altruism from PH would backfire. (1/)
@sunsweptforest For the first 2-3 papers, we tried our luck at the big name journals. They would sit on the manuscript for a month and then send a form-letter rejection. Meanwhile, they were fast tracking review and publication of “good news” papers on the exact same topics (2/)
@sunsweptforest Science, in particular, actively promoted the idea that immunity to covid would be long lasting.

For example, our paper (preprint in fall 2020) on the outcome of a “vax & relax” strategy made a bleak prediction- “making COVID-19 the third leading cause of death in the US” (3/)
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Read 12 tweets
Nov 14, 2023
This point has been before, but if you want to know what the future holds for long Covid, look to high-contact-rate professions.

In the UK, the Guardian noted the shortage of workers specifically in this category (1/)
If you think of high-contact-rate professions in the US, ones where people are likely to come in contact with Covid, what are they? Childcare workers, bus drivers, nurses, pharmacists, prison guards, for example? (2/)
So how’s the labor situation working out in these professions? Chronic and nationwide shortages in each of these categories, showing no signs of abating and in some cases, the worst that they have been since the beginning of the pandemic. (3/)
Read 16 tweets
Nov 4, 2023
Grimly fascinating thread on the way in which the murderous Tory response to covid was shaped by advisors who believe in (surprise, surprise!) eugenics (1/)
“Covid is just nature’s way of dealing with old people”. Can’t make this shit up. It explains why, as groups like ours were warning about the negative consequences of a negligent covid policy, governments such as UK were actively pursuing such policies (2/)
The tsunami of death and disease that would inevitably follow from such poor choices represented success to these politicians. Far from being an unanticipated failure. They knew all along. (3/)
Read 4 tweets
Oct 24, 2023
Taking Paxlovid in this study was associated with a minuscule reduction in risk of long Covid. Note that the article is written in a way to make that less obvious. (1/) cidrap.umn.edu/covid-19/resea…
While the article is focused on inequity, the magnitude of the effect size (reduction in LC risk upon taking Paxlovid) is so small that you have to squint to see it (2/) Image
Their classification of “Covid” patients was based in part on whether the patient took Paxlovid. If you look at the subset of patients who were definitively diagnosed with Covid, the hazard ratio is 0.94.

A ~5% reduction in relative risk of getting LC is not meaningful (3/)
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Read 4 tweets
Oct 24, 2023
@white_bite @xabitron1 @G_Commish @NjbBari3 @DavidJoffe64 @PDAquinas @0bj3ctivity @LauraMiers @HarrySpoelstra @MeetJess @ejustin46 @elisaperego78 @1goodtern @RadCentrism @AndrewEwing11 @outbreakupdates @AltenbergLee @C_A_Gustave @Alitis__ @CarlvKeirsbilck @TRyanGregory @kasza_leslie @SGriffin_Lab @fitterhappierAJ @tohmes1 @DrJohnHhess Umm. I see it very differently, I guess. The confusion arises from the difference in evidentiary standards required to call something a “probable carcinogen” vs a “possible” or “known” carcinogen (1/)
@white_bite @xabitron1 @G_Commish @NjbBari3 @DavidJoffe64 @PDAquinas @0bj3ctivity @LauraMiers @HarrySpoelstra @MeetJess @ejustin46 @elisaperego78 @1goodtern @RadCentrism @AndrewEwing11 @outbreakupdates @AltenbergLee @C_A_Gustave @Alitis__ @CarlvKeirsbilck @TRyanGregory @kasza_leslie @SGriffin_Lab @fitterhappierAJ @tohmes1 @DrJohnHhess We know that sc2 causes DNA double strand breaks and chromosomal instability. Any agent that causes those outcomes is carcinogenic, provided that the dose used in the studies is relevant to human exposures in the real world (2/)
@white_bite @xabitron1 @G_Commish @NjbBari3 @DavidJoffe64 @PDAquinas @0bj3ctivity @LauraMiers @HarrySpoelstra @MeetJess @ejustin46 @elisaperego78 @1goodtern @RadCentrism @AndrewEwing11 @outbreakupdates @AltenbergLee @C_A_Gustave @Alitis__ @CarlvKeirsbilck @TRyanGregory @kasza_leslie @SGriffin_Lab @fitterhappierAJ @tohmes1 @DrJohnHhess But this is a virus, so the question of dose doesn’t arise. The likelihood that the in vitro studies used a “dose” that was too high is pretty much zero. That eliminates the primary reason for translational failures (3/)
Read 14 tweets

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