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What we still don't know for both Pfizer/BioNTech and Moderna vaccines:

"A vaccine that prevents infection entirely provides indirect protection to others. If I can't get infected, I can't infect you. But it is possible to have a vaccine that prevents disease but individuals can still be infectious." (1)

In that case, those at risk are only protected when they receive a vaccine, but still aren't when just those who they are in contact with received it.

"Most Phase 3 trials are measuring efficacy to prevent disease as the primary analysis" (2)

Not infection.

The whole thread with more details, already written in September, before both announcements:

https://twitter.com/nataliexdean/status/1310613702476017666

by: "Natalie E. Dean, PhD, Assistant Professor of Biostatistics at @UF specializing in emerging infectious diseases and vaccine study design. @HarvardBiostats PhD." (3)

1) https://twitter.com/nataliexdean/status/1310613711808278528

2) https://twitter.com/nataliexdean/status/1310613708557692928

3) https://twitter.com/nataliexdean



It would seem at least reasonable to hope that one follows from the other. If our bodies fight the virus effectively, the viral loads we would shed ought to be lower. The period where high virus loads are found in our bodies will be shorter, requiring less hospitalisations, and thus chances to give it to other vulnerable people.

There are of course lots of hypotheticals here, and things to be concerned about, but a priori surely we should be hopeful it reduces infections too?


Your assumption:

> The period where high virus loads are found in our bodies will be shorter

is precisely what can't be assumed in advance but must be measured, as there are known examples where the assumption doesn't hold at all (and that includes the flu vaccines).

(Not to mention that just "shorter" is by definition not "sterilizing", the transmission is then obviously still possible.)

If the virus is transmitted via the upper respiratory tract, and it is, it's less probable that the immune cells in blood can prevent the infection and viral shedding of the mucosa. The cells have to be first attacked and infected before the immune reaction can kick in. Even now, it is known that the highest infectiousness of SARS-CoV-2 is often before the symptoms are observable, i.e. before the immune reaction starts. That would also explain the existence of asymptotic carriers: their immune system already protects them, but they are still able to infect others.


Does this mean that if a lot of people refuse to take the vaccine then we could still be dealing with masks, social distancing and lockdowns to protect those that refuse the vaccine?


Maybe, but at some point it is their own stupid fault.

The real question is the 5-10% that the vaccines don't work for - are they completely unprotected and we should wear a mask to protect them, or does enough protection exist such that they only get mildly sick vs die. There isn't enough evidence yet, but what we have suggests the former.


That's an additional problem, also known from the flu vaccines: some of those vaccinated just can't develop enough immunity to be protected, and unfortunately there are more of such among the older population. We also don't know the numbers for that population for these vaccines.

I worry also for the times during which there are not enough vaccines for everybody who is willing to get one. And also for the times when the immunity by those vaccinated vanes -- in other vaccines that also happens faster among those who are older. These numbers we can't have now anyway, that will by definition take much more time to be known.


The Moderna news today suggests there is protection to reduce the severity, although limited data so far.




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