This is saying that 40-60% of existing immune responses (learned over many years of previous coronaviruses) are also protective against the SARS-Cov-2 virus which causes Covid-19 disease.
There is a time-based arms race between virus replication & immune defense. If these subjects are otherwise healthy, their immune system should have a good chance of clearing the Covid-19 virus successfully, because it has a "running start" against the new virus.
After recovery, their adaptive immune system should have developed an additional immune response that is customized to defend against Covid-19.
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.
"Whether this immunity is relevant in influencing clinical outcomes is unknown, but it is tempting to speculate that the crossreactive CD4+ T cells may be of value in protective immunity, based on SARS and flu data."
https://twitter.com/profshanecrotty/status/12610523537733632...
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.
Since corona viruses are quite common it will be hard to know which one causes this immune response.
The interesting part is that early on tests of MERS and SARS survivors didn’t indicate an adaptive immune response against COVID-19.
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.
80,000 Americans died, and thousands more will die before this is over.
Which numbers would those be? Because I'm looking at https://coronavirus.jhu.edu/data/new-cases, and it does not in any way support your claim.
Remember: the correct recation to a situation like this will probably look like an extreme overreaction.
There is basically no way of telling the adequate response from a complete overreaction right now.
Even if it turns out that in the end the IFR of the disease was just 0.1%, or that 50% had existing immunity... then that will only change after the fact what would have been the correct response. The decision needs to be made without that information.
But I've read that most common cold immunities last only for a handful of months or years, not decades.
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.
> The average adult gets two to three colds a year, while the average child may get six to eight
> Other commonly implicated viruses include human coronaviruses (≈ 15%),
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.
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.
OTOH, the killer feature of Covid-19 seems to be triggering an out-of-control adaptive immune response. That's probably why kids aren't dying, as their adaptive immune response is still developing.
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.
Wrong. There are 200+ strains of various viruses that are all lumped together as the "common cold" only 4 of which are coronaviruses. The vast majority of common colds are not coronaviruses.
It's not saying that. The presence of these antibodies does not necessarily mean any level of immunity against SARS-CoV-2, which is a different virus than the one that triggered these antibodies. The degree to which these antibodies contribute towards immunity against the new virus is unknown, and wasn't evaluated by this study.
Most explanations I’ve seen is the fatality rate increase with age from a small factional percentage to 10% in those in their 70s and 80s.
That combined with the proximity of people at a nursing home make it especially deadly.
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.
