SARS-CoV-2 seroprevalence in healthy blood donors during Covid-19 Milan outbreak

> For whatever reasons

Perhaps because he was making baseless claims about his teammates and tainting the reputation of the club. He should at least know that players being taken down by cold or flu is not unusual in football.

2014 Seven players are struck by 'flu symptoms': https://www.telegraph.co.uk/sport/football/teams/germany/109...

2017 Wenger fighting to contain outbreak: https://www.dailymail.co.uk/sport/football/article-4296828/N...

Feb 2019 'Man flu'[0] sweeps through League Two club: https://www.bbc.com/sport/football/47239534

March 2019 'epidemic' with eight players: https://www.thesun.co.uk/sport/football/8709002/poland-flu-e...

[0] https://en.wikipedia.org/wiki/Man_flu

Did the players test positive for Cov2 antibodies?

We should expect to get serological data from excess Chinese mortality before December then. Assuming they agree to good back sampling. They have biopsies like any public health system.

We know #2 is true for younger people, as the mortality rate is almost zero unless you're in a nursing home.

Why not the fact that perhaps the virus found its way in more vulnerable populations, such as hospitals and nursing care homes (44% of the current deaths)?

If that happened, the population would be very largely skewed towards the most vulnerable (you usually don't go to ER or a hospital if you're healthy) and that would explain the uptick in deaths.

There's no other idea I can offer to explain why a disease with an estimated IFR between 0.5 and 0.9% would cause an order of magnitude more deaths.

4. The current beliefs about lethality and R0 are way off

It's also possible that people happened to develop antibodies for a different coronavirus that are also effective against SARS-CoV-2-- meaning they're true positives (effective antibodies) that don't indicate an infection with SARS-CoV-2.

This happened with someone that survived SARS-CoV having effective antibodies against CoV-2: https://www.nature.com/articles/s41586-020-2349-y

What if this "exponential explosion in deaths" is because people didn't receive medical care for various other conditions and thus deaths spiked?

#3 sounds both plausible and absolutely dreadful to me (I’m in Sweden where the de facto “strategy” is still herd immunity)...

#1 and #2 sound not entirely implausible to me though... Severity of disease seems to vary a lot with infection dose. Is it really that far fetched that when infection doses are very low the disease is mild, but as the virus level in the population rises and infection doses go up the disease becomes a very serious public health issue?

Does anybody know any data that supports/refutes my thinking above?

>That is an unlikely hypothesis, given that we didn't see an exponential explosion in deaths

The unmitigated doubling time of COVID-19 seems to be around 2.5 days. So if about 1% gets hospitalized and people noticed after 10 or so patients with the same symptoms (that's before any of them died, mind you) you'd need about 1000 people infected. To go from 1 infected person to 1000 takes log2(1000)=9.96 doublings. So if the doubling time is 2.5 that would be 25 days or over 3 weeks before anyone would notice.

Some of these numbers are a bit of a guess but I'm trying to show that "exponential explosion" can be very small and slow at the very beginning of an outbreak.

I like #3 too. And really it is worth waiting for expert opinions rather than getting too excited - maybe people develop antibodies in response to some other cold virus that has a similar external surface to COVID-19. Who knows? The world is large and there is a lot going on. These 98 and 100% style test sensitivities don't magically make the world a controlled lab-like environment. I'm willing to bet crazy things sometimes happen that weren't tested in labs.

I can't find it anymore but there was an article here published a few days ago that essentially estimated whether infections with SARS-CoV-2 come from homogeneous transmission, i.e. everyone who has it infects a few people, or from highly concentrated transmission, i.e. there are a few people who infect a large number of others. The latter seems to be the case for SARS-CoV-2. This to me makes me believe 2. is correct. We know that this disease is non-lethal for the large majority of people below 40-50. It is thus not unthinkable that it was able to spread widely in those groups before finally hitting more vulnerable parts of the population all at once in March, leading to the devastating effects we observed. Additionally, in a model where everyone is equally likely to be infected, the number of deaths would reflect the percentage of people having the disease. That is why people think there is an upper limit of a few percent of infected. This however breaks down entirely if there are clusters of cases within different subpopulations.

It is not #3, if we believe what they say in the study:

"The test had a 98.3% specificity and 100% sensitivity"

I.e. only 1.7% likelihood of false positives

EDIT: And no case was missed

I'm betting we didn't see an exponential explosion in death - ever. Look up the gompertz curve. It's very convenient for politicians to have everyone believe counterfactuals of unbounded exponentials.

With what we know of the age dependence of the CFR, it is not unreasonable to think #1. In fact, until it broke into long term care facilities, it would fly under the radar fairly well.

Remember, for #2, it is not that most people stay asymptomatic. They are usually pre-symptomatic, and do have the symptoms later. Just for the majority of folks <60, they are a bad cold. If you are under 20, not even a bad one.

And from some comments down thread, #3 is as likely to be wrong with these having more false negatives. So, tough to say.

Prior to about the 21st of Feb Italy only reported three cases of coronavirus in the entire country with the most recent case being a Wuhan evacuee at the start of the month: https://uk.reuters.com/article/uk-china-health-italy/first-i... As you say they started to lock down very soon after that. February 24th is very much at the start of the detected outbreak, and it seems safe to conclude that the virus was indeed already circulating widely at that point. They went from basically no reported cases to the most cases in the world outside China and their healthcare system being overwhelmed in days.

While other experts had pointed out that Italy likely had more cases than already reported, the numbers they threw around were more in the hundreds range rather than substantial percentages of the entire population: https://www.nytimes.com/2020/03/21/world/europe/italy-corona... This does explain a lot though, both about what happened in Italy and why containment efforts in other Western countries failed whilst ones closer to China geographically seem to have done much better.

It's anecdotal, but if you follow https://www.reddit.com/r/COVID19positive/ there are tons of similar anecdotes. In a large enough number anecdotes make a statistic.

Also, I claim that there was not even time to test the reliability of the serological tests an actual patients. So, anecdotes may be all data we have.

I was a test against IgG antibodies. The report does not mention the manufacturer of the test.

Well no, but also in the US there are research facilities working with Coronaviruses [1]. I am not advocating for this theory because there is zero credible evidence for it but there are scenarios that would make this theoretically possible.

[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4797993/

Did you realize that there are also bats in Austin, Texas? They live under the bridge there.

Unless these bats are perfectly clean and disease free, after millions of years of evolution. And somehow, only the bats in China, can carry a novel coronavirus?

I’m just pointing out that bats exist worldwide. And they can infect other farm animals. This is not a unique situation to only China.

This is far from certain. The virus has not been identified in the wild. There are several genetically similar viruses in pangolins and bats sampled from China, but Covid combines sequences from at least 2 of them.

I don't think it has anything to do with corruption and terrible healthcare (mistakes were made, but as a resident there, I think the system works pretty well nevertheless, or at least used to be pre-crisis).

I think it has more to do with the route of entry of the virus in the territory, which hit hospitals first (not closing down Alzano Lombardo was a grave mistake), then retirement homes (an error shared with Lazio and elsewhere).

This meant that the newly-infected population was largely skewed towards the most vulnerable, and coupled with imperfect knowledge about treatment, the net result was a lot of deaths.

If this is true, wouldn't that mean that the R is in fact not as high as we believe it is, because it was spreading for longer on a slower rate as opposed to spreading fast in a shorter time period? If we think that it is still highly infecious then the only other conclusion can be that we have a much larger population already immunonised?

If that were the case, then since hardly anyone was sick, hardly anyone should have had antibodies.

Unless, of course, the antibody test is too general, and is picking up false positives, or antibodies that have nothing to do with COVID.