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naraburns  nihil supernum  2yr ago (text post)   33194 thread views

Culture War Roundup for the week of October 10, 2022

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I thought literally everyone at the time said that the purpose was to reduce severity in most patients

The scientists said that they were only testing for proving making individuals less likely to die, which they were very good at in the pre-Omicron days.

A bunch of other people, particularly in the media, showed up and said "well, that must mean it reduces transmission, right?" and then said "it obviously reduces transmission" even though the scientists said they never tested proved that.

This is some alternate kind of motte-and-bailey, where the useful idiots say wrong things that you can claim credit for in case they turn out to be right, but disavow if they are wrong.

This is some alternate kind of motte-and-bailey

"Distributed motte-and-bailey" is the term that seems most popular.

A bunch of other people, particularly in the media, showed up and said "well, that must mean it reduces transmission, right?"

I could swear it was actual scientists pointing out expected reductions in R (albeit with huge error bars). And I wouldn't say they were wrong to! It would be wrong to say that reducing detectable infection rates must reduce infection-and-retransmission rates, but that's still the correct prior to have in the absence of more direct (and much much harder to obtain) evidence.

they were very good at in the pre-Omicron days.

Now this is where priors seemed to be getting ignored. "Optimal virulence theory says mutations which spread fast will outcompete merely-more-lethal variants" might not have been a prior to hold strongly, but the objections I saw weren't just "that's the null hypothesis but we shouldn't just assume it will certainly be true", they went as far as "coronaviruses have a gene-proofreading function, we shouldn't assume they will mutate at all".

The scientists said that they were only testing for making individuals less likely to die, which they were very good at in the pre-Omicron days.

No, this is not what was stated, not what was requested by the FDA, and not what anyone believed about vaccines at the time. Here's the FDA guidance for development and licensure from June 2020. Scroll down to page 13 and start looking through the Efficacy Considerations section:

Either laboratory-confirmed COVID-19 or laboratory-confirmed SARS-CoV-2 infection is an acceptable primary endpoint for a COVID-19 vaccine efficacy trial.

This is pretty normal, what everyone would have considered the bog-standard endpoint until the Covid vaccine retconning started up. You check whether the vaccine prevents infection and you get a double-whammy - can't die from something you're not infected with and can't infect other people with something you're not infected with.

As it is possible that a COVID-19 vaccine might be much more effective in preventing severe versus mild COVID-19, sponsors should consider powering efficacy trials for formal hypothesis testing on a severe COVID-19 endpoint. Regardless, severe COVID-19 should be evaluated as a secondary endpoint (with or without formal hypothesis testing) if not evaluated as a primary endpoint.

This phrasing makes zero sense if the expectation was that the only thing anyone would test for is whether vaccination impacted severity. Severity was worth checking as a secondary endpoint precisely because it's possible that you'd impact severity without impacting likelihood of infection and transmission, but this would generally be considered a disappointing result.

Of course, that might just be what the FDA wanted to see and the companies weren't able to meet that criterion, or elected to go with other study designs. We can look at the original December 2020 emergency approval of the Pfizer vaccine though:

First primary endpoint: COVID-19 incidence per 1000 person-years of follow-up in participants without serological or virological evidence of past SARS-CoV-2 infection before and during vaccination regimen – cases confirmed ≥7 days after Dose 2

Second primary endpoint: COVID-19 incidence per 1000 person-years of follow-up in participants with and without evidence of past SARS-CoV-2 infection before and during vaccination regimen – cases confirmed ≥7 days after Dose 2

Severity shows up under the secondary efficacy endpoints. Their results:

For participants without evidence of SARS-CoV-2 infection prior to 7 days after Dose 2, VE against confirmed COVID-19 occurring at least 7 days after Dose 2 was 95.0%. The case split was 8 COVID-19 cases in the BNT162b2 group compared to 162 COVID-19 cases in the placebo group (Table 6). The 95% credible interval for the vaccine efficacy was 90.3% to 97.6%, indicating that the true VE is at least 90.3% with a 97.5% probability, which met the pre-specified success criterion.

The specificized success criterion was preventing infection. The stated effect was preventing infection. Anyone that now tells you that the scientists were only testing whether it made individuals less likely to die is badly misinformed or is telling a whopper.

Thanks for the specific quotes. I'll save this one to reference it.

You are saying "stops infection" where I am saying "stops transmission."

I guess when I said "only testing" I should have said "only proving."

What is the proposed mechanism for transmission without infection?

You are looking at "how do you get A without B" when I am looking at "given B can we stop A" which is a different thing.

Putting aside the logical incoherence of transmission without infection, I'm at least glad we can agree that your original claim that "scientists said that they were only testing for making individuals less likely to die" is demonstrably a retcon.

Putting aside the logical incoherence of transmission without infection

Yes, the thing that I never said, it is logically incoherent. Yes.

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