40-60% of the unexposed produce Covid-19 antibodies due to earlier cold exposure [pdf]

Yet we decimated our economy out of an absolute panic and still continue to push for lockdown even when numbers show it’s time to start things again.

The extent antibody-dependent enhancement causes mortality is questionable. Ongoing studies (https://clinicaltrials.gov/ct2/show/NCT04324021) to treat cytokine storm cases will hopefully be able to better estimate it.

Existing cross-reactive adaptive immune cells or antibody != protection from this new virus. It only shows that these viruses are similar so there is some cross-reactivity from immune cells and antibodies designed to detect some viral epitopes (not terribly surprising). The question of whether these CD4+ t-cells that cross react are protective in humans would still need to be determined. (ie, what you’re saying is possible but not at all a foregone conclusion).

The possibility of ADE mentioned in the discussion, for example, would actually mean that some cross-reactivity (in this case of antibody) could actually cause very severe disease in those individuals. This, by the way, would also be a good explanation for why more naive individuals to all human coronaviruses (ie children) do not generally get as severe of disease.

Importantly this is a T cell study not exactly an antibody assay study (t cell responses are a prerequisite for antibody responses).

I don’t understand the paper well enough to even try to check the statistics (if there is any; I didn’t see clear claims, so this may just be a ‘here is what we observed’ paper), but you can’t disqualify a paper on sample size alone.

20 can be large enough if the effect is large enough. For example, if you do heads/tails 20 times with a fair coin, the probability to get more than 15 heads is less than 1%, so if you get, say, 17, the hypothesis that the coin is fair can be rejected.

The implication (in the best of all possible worlds) is that the antibodies that fight common cold also fight COVID-19. Or it could be a simple correlation and not significant.

What is paper is saying is that previous exposure to coronavirus (the common cold) grants some level of immunity to covid19.

But there is something that works in the opposite direction: if those with some protection become asymptomatic or mildly symptomatic but are still spreaders, then their lack of symptoms might mean they move around more and have more contacts, outweighing their smaller level of infectiousness. We can't know.

If those with existing protection can't become spreaders, then it should indeed mean that the R0 is much higher than expected (It was estimated from doubling assuming 100% were initially susceptible, so if only 50% were initially susceptible then the estimate would be off by a factor 2). But I don't think that this is what the paper is saying. It's saying that some have partial immunity responses that deal with the infection. They still get immunity after their infection, not before.

If they interact regularly with family and were long exposed to commonly circulating viruses (e.g. from kids), they would have a resilient/diverse immune system. This assumes a healthy diet with no deficiencies (Vitamin C, D, Zinc).

Another complicating factor is the content of flu vaccines.

I had the same question when it all started: how exposure to other coronaviruses affects the response to SARS-Cov-2, and what does it mean for people with different history of exposures.

One hypothesis was that older people have a higher probability of dying because their immune system does not produce antibodies fast enough to keep up with the virus. The other one was the complete opposite: that due to the long history of exposures to other coronaviruses they have too much of a response and cytokine storm as a result but that does not seem to be the case.

But I've read that most common cold immunities last only for a handful of months or years, not decades.