Does this mean that it was much more contagious than thought, if it spreads so fast while so many already have some immunity? Also, if 1/4 of New York City has already had covid-19, then maybe there is only ~1/4 left who wouldn't have immunity. Which would imply that if all restrictions were lifted (in NYC) the "curve" of new infections would be much lower than the first one.
Does this explain asymptomatic cases? Maybe people don't develop symptoms because they have cold-related antibodies that don't let COVID develop. Can these people still shed and transmit SARS-CoV-2?
The response was primarily by Th cells, not the TC cells, so yes, this isn't immunity, but it would speed to body's adaptive immune system response.
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.
It means that people that have the at least one common antibody from exposure to the common cold as those that have had COVID-19.
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.
No it doesn't mean that at all. What this is telling you and what media has been avoiding saying is that coronavirus is a family of viruses that make up the common cold. It's not the only virus that's lumped in as the common cold but it is one kind. Coronavirus isn't new, covid19 is just a previously unknown variation.
What is paper is saying is that previous exposure to coronavirus (the common cold) grants some level of immunity to covid19.
> coronavirus is a family of viruses that make up the common cold
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.
> What is paper is saying is that previous exposure to coronavirus (the common cold) grants some level of immunity to covid19.
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.
The effective R is R(0) multiplied by (among other things) the susceptible population. If those with existing protection are still susceptible and still become infectious when infected, then this does't change the evolution. It's likely that those who are infected but have some immunity develops a less severe illness, which is possibly less infectious.
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.
> Importantly, we detected SARS-CoV-2−reactive CD4+ T cells in ~40-60% of unexposed individuals, suggesting cross-reactive T cell recognition between circulating ‘common cold’ coronaviruses and SARS-Cov-2
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.
And that's with the lockdowns. The figures could easily be an order of magnitude or more worse be now without them. We successfully managed to not exceed the capacity of our healthcare system, for the most part.
There is still a piper to pay for the lockdowns, and that is the patients who will die due to untreated heart disease, missed cancer treatments and surgeries, mental health problems, und so weiter. Not to mention all the people who will now find their disease at a later date and suffer a worse prognosis for it. The lockdowns could have created more deaths and suffering than were prevented, but we won't know for some time.
Social distancing was always going to happen. Restaurants here in NYC were running at one quarter their normal business in the days leading up to the official lockdown. People aren't stupid, and will choose to stay home when a pandemic is ravaging their community regardless of what official guidance might be.
There's no world in which the pandemic is running unchecked through society and people are acting like everything is fine and normal and doing all the usual stuff they're accustomed to.
This is a conflation of what the virus itself has down, and the response to it.
Not at all. Hospitals shut down elective procedures, not because they were running out of room, but because they were ordered to do so. That freed capacity may have been necessary in NYC, and maybe not, but nowhere else was it necessary.
At the expense of all other medical procedures that people needed, let us not forget. We did all of this despite a whole bunch of people effectively having already been vaccinated against COVID-19.
No, they're saying that 40 to 60% of people have antibodies that can make it easier to fight Covid-19... this could be one of the reasons the elderly die more often for example.
However, for perspective, North America (which is mainly the US) has had 1.65M cases and 100K deaths, while Europe has had 1.76M cases and 161K deaths.
With all the focus on the US as the single country with by far the most cases, it seems to have not registered with most people that Europe as a whole is of comparable size, has had a comparable number of cases, and has seen a lot more casualties.
I wouldn't draw the conclusion that this validates the US health care system, or the decisions of authorities, because of other variables, but it makes me wonder if a narrative about how terrible the US is has been allowed to obscure the facts.
if we had not locked down everywhere would have been like italy or nyc or worse. remember that deaths peaked at 2500 per day in the usa with a lockdown. thats 5x of a bad flu season with no lockdown.
I'm in NYC and our biggest problem here is that our dumbass mayor and governor waited at least a week too late to shut everything down. If we'd locked down sooner we'd have had a lot fewer deaths and would be much further along the road of reopening already. One week on the front end is worth many weeks on the back end when you're talking exponential growth.
NYC and surroundings are very different than FL are very different than California. I agree NYC was a complete disaster, but it doesn't follow that Dallas would have met the same fate.
Classic conflation of the effects of a pandemic itself with the measures taken to fight it. Things would not be going along swimmingly if governments hadn't stepped in with social distancing measures; instead there'd be a lot more dead and everyone wouldn't be leaving their home anyway out of raw fear.
Sweden begs to differ with this statement as the as the misleading headline article from the NY times shows that their numbers aren't meaningfully different than other European countries which did lockdown. UK which has a lockdown policy was quite a bit higher.
CDC own numbers on this aren't really supporting the panic level either.
Pneumonia is still stomping covid19 as far as deaths. Death projections are made from the 2017-2019 data and as of now they're at 101% of their protections. That number moves up and down but has been sticking really close to 100%. With 60+k unexpected covid19 we should be around 105-107% deaths but we're not.
Things aren't over yet but all the be data coming out is very much supporting that is has been a massive overreaction. If we're going to overreact for the purpose of saving lives, why don't we don't we do it to solve the 9.1 million deaths from hunger and hunger related issues?
I have a question on this regard, since my digging didn't find anything. Is there any correlation between where the first clusters of cases where found (schools, hospitals, offices, houses...) and the subsequent hit on the health system?
Maybe, just maybe you shouldn't look at new cases as your measurement when you are constantly ramping up testing. If you test more people of course you will find more people with the virus. You should be looking at hospitalizations and those numbers are pretty much down across the board.
An alternative way to look at this is that you shouldn't remotely consider reopening if you don't even have enough testing capacity available to identify nearly every case. You can't control outbreaks if you don't have the data needed for contact tracing.
Why is that? I don't see the need for testing when we already know that folks under 60 are usually fine if they take the standard precautions, and everyone over 60 or in a risk group should remain isolated.
The testing is nice to have, but shouldn't really alter people's behavior.
It's pretty clear that a positive test is the early symptom for a large percentage of people.
It's also not the interval immediately after infection takes place (your hour later) that matters, it's the period starting a few days later. Get them out of circulation before they have a chance to spread the virus and we can slow it down further than we have till now, even with more activity taking place.
If you look at % positive it accounts for increases in testing ability. So are you just testing more, or are you actually finding an increase in cases in your sample of the total population. That is what they're looking at to get a true determination of if the infection rate is increasing, decreasing or flat.
For most of the United States the total lockdown has been overkill. A better way to compare the US to most European countries would be to compare individual states and even then some states have rural populations that would have been fine without lockdowns. For example, New York City is one of the hardest hit cities but the rest of the state of New York has had significantly less cases and deaths. Is this because of the lockdowns? Probably, but at the same time our hospitals have not been running at capacity or even close to that (some have even furloughed workers because all elective procedures have been cancelled).
If the goal is to find a cure before we lift lockdowns we better do something to help those economically impacted by them (and giving away free money is not a viable option). If the goal is to not overwhelm our healthcare systems we are doing that great but a country wide lockdown is not viable either. The New York Times has a good map [0] to show how little most of the country has been affected. That is why state governments should be handling the outbreaks in their own state instead of shutting down the country all together.
These lockdowns were implemented because we had no idea how this virus worked or where it was. We have a much better idea now and each state can act accordingly.
Georgia is a good example of a state that has started to open it's economy and is still seeing a decline in new cases. NPR has been tracking state restrictions and Georgia lifted some restrictions April 24[0] more restrictions were lifted May 1
Georgia's cities and counties mostly put their own measures in place without waiting for the governor to decide to do something. I don't think they're waiting for or depending on the state's call on it.
Well to a large extent that’s policy driven as well. The media have been pounding the message safer at home unrelentingly for weeks. Make no mistake, the virus is real, it is far more deadly than the flu, and while there’s no natural experiment it’s likely the lockdown saved lives.
That being said, the messaging hasn’t been calibrated very well.
Everyone talks about the post 9/11 “security theater” of the TSA, but because we’re unable to reasonably assess the threat, today we’ve got equivalent public health theater, but the TSA is us.
> 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.
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.
Yes, look at Greece, they implemented extreme measures.
As a result, they basically had no issues at all with the virus compared to neighbouring Italy and Turkey.
And look at Japan, where they half-assed their response and turned out better (fewer deaths per capita) than Greece. I think most commentary assigns way too much credit/blame to the government's response, while ignoring yet-unknown environmental, pre-existing cultural/behavioral, genetic, or other factors. I'm saying this not to excuse government incompetence, but to counter the persistent suggestion that everyone could have the same good result as e.g. South Korea if only their government had responded in the same way.
This opinion would be adorable if it wasn't so dangerous. Every major area in the USA outside NYC and Washington is still growing in cases. It hasn't nearly peaked.
My point still stands. The major areas still growing in cases shouldn't ease up. Anywhere that has peaked and is declining can start to ease up and continue to monitor the situation. We shouldn't require everyone in the country to wear a coat because it's cold in New York City.
What do you think would happen to the economy if we let the virus run free through the population, and eventually everyone would be too scared to leave their house and quit showing up to their job?
>After recovery, their adaptive immune system should have developed an additional immune response that is customized to defend against Covid-19.
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.
> 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.
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.
Yes, as one of the authors said on Twitter, this doesn't prove anything about the effects on SARS-CoV-2 immunity, but it is suggestive:
"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."
What if we infected people purposefully with common cold coronaviruses to help them get a level of immunity? Common cold isn't fatal or dangerous right? Could this work as a 'vaccine' or prophylactic? You wouldn't even need to test people with this test before doing that because the people with immunity will just not get sick with the cold.
From what I've read, immunity to other coronaviruses typically only lasts a year or so. SARS hasn't infected anyone in over a decade, and it's been a few years since a MERS outbreak.
Yes, but they could have other risks due to existing medical conditions. It's an arms race between the speed of replication of the invading virus, and the immune system's ability to respond. Existing conditions add many complications.
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.
The term "flu vaccine" is as meaningful as "glass of liquid". Depends what's in the glass. The content of vaccines vary across geographical regions and their very purpose is to interact with the immune system. The precise contents of previous vaccines should be tracked and analyzed in studies of elderly immune system responses to SARS-Cov-2.
Disclaimer: not an immunologist, no formal post secondary biological education, my thoughts on this are likely worthless.
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.
AFAIK it depends on how long lived the antibody response is. Memory cells can last different amounts of time for different infections, or (like for certain calicivirus infections?) hardly develop at all. Have no nice paper on hand to back this up though. But if it's a short lived response (as in years, not decades), it's good to be freshly exposed and like another commenter said, kids get colds all the time. And likely parents of young children too (I know I did). Maybe that helps?
Many older people were immune to the Spanish Flu because they had been around long enough to have developed antibodies for a similar strain decades before.
But I've read that most common cold immunities last only for a handful of months or years, not decades.
How do they know for sure people have not been exposed? I don’t see how you could prove definitively that a person wasn’t. And with many cases being asymptomatic they could have had it long ago and not known.
Right. Blood from 3-4 years ago has antibodies. One interpretation could be that those people were never exposed but somehow have antibodies which needs investigation. Another interpretation could be that covid-19 is a particularly bad seasonal strain of a disease that has been around for a long time. We probably will never know. People are still studying SARS and MERS.
There seem to be other reasons too, apparently the activity of Antigen Presenting Cells (another cog required in the production of the immune response) deteriorates with age, as pointed in this papers introduction section.
This seems weird to me though. New Yorkers should have wide exposure to the common cold due to density, as would people in Wuhan.. why was this sars-cov2 so lethal then?
More than 1/3 the fatalities in NY were in nursing homes. Nursing homes in NY were required to readmit recovering patients coming back from the hospital. Thanks Gov. Cuomo!
Nursing homes account for 70% of fatalities here in Quebec! And retirement homes 20%. It's very telling that we shut everything up here, with very intense measures compared to our neighbors, but we just utterly ignored nursing houses. We were giving fines to 13yo kids playing soccer in parks when nursing home patients were still going in and out freely and their caregivers were encouraged not to wear PPE (not that it was available anyways, it was mostly diverted to hospitals...).
New york did a similar mistake by forcing nursing homes to accept recovering COVID patients, with disastrous results too.
If I understood it right they checked that against two groups of 20 people (40 in total only). The study itself seems super interesting and important but such ridiculously small sample size to me, a layman following COVID-19-related research. Is 40 acceptable in this case? Since they are on Cell.com I suppose it is. Bad sample size in COVID-19 research has been discussed recently already and it is a known problem. Another thing is that the sample size was a hidden lead in page 3 and a figure shown only in page 11 of the paper. I wish scientific papers had something of a "nutrition facts" label with basic info like that in their first page.
This is not a clinical trial though, merely a mechanistic study. The types of assays they have done typically take years to get right with just a handful of samples so it's actually quite impressive.
Importantly this is a T cell study not exactly an antibody assay study (t cell responses are a prerequisite for antibody responses).
Yes, the paper could’ve been written better. The normal presentation order is abstract-introduction-methods-results-discussion. Here, they mix the methods and the results/hide the methods inside the results.
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.
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[ 0.24 ms ] story [ 79.4 ms ] threadSo those asymptomatic might simply be people whose natural lung operation is strong enough that they can compensate for the covid damage.
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 the only virus that's lumped in as the common cold but it is one kind.
Perhaps not having knee jerk reactions and careful examination of the information is what's needed.
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.
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.
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.
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.
There's no world in which the pandemic is running unchecked through society and people are acting like everything is fine and normal and doing all the usual stuff they're accustomed to.
This is a conflation of what the virus itself has down, and the response to it.
There is no vaccine against COVID-19... unless you consider drinking bleach or dying...
The actual deaths we've seen and the overwhelming of hospitals in multiple countries refute the kind of narrative you're fantasizing about.
The loss of a loved one is never temporary.
However, for perspective, North America (which is mainly the US) has had 1.65M cases and 100K deaths, while Europe has had 1.76M cases and 161K deaths.
With all the focus on the US as the single country with by far the most cases, it seems to have not registered with most people that Europe as a whole is of comparable size, has had a comparable number of cases, and has seen a lot more casualties.
I wouldn't draw the conclusion that this validates the US health care system, or the decisions of authorities, because of other variables, but it makes me wonder if a narrative about how terrible the US is has been allowed to obscure the facts.
The stats I was looking at appear to be based on a definition of Europe that is about 700 million, while "North America" is about 590 million.
CDC own numbers on this aren't really supporting the panic level either.
https://www.cdc.gov/nchs/nvss/vsrr/covid19/index.htm
Pneumonia is still stomping covid19 as far as deaths. Death projections are made from the 2017-2019 data and as of now they're at 101% of their protections. That number moves up and down but has been sticking really close to 100%. With 60+k unexpected covid19 we should be around 105-107% deaths but we're not.
Things aren't over yet but all the be data coming out is very much supporting that is has been a massive overreaction. If we're going to overreact for the purpose of saving lives, why don't we don't we do it to solve the 9.1 million deaths from hunger and hunger related issues?
The main difference is that they have a lot more deaths relative to many other countries that handled social distancing better.
No, the UK was following in Sweden's footsteps until forecasts became untenable, by which time a lot of damage had been already done: https://www.technologyreview.com/2020/03/16/905285/uk-droppi...
Compared to its neighbours, Sweden is doing remarkably bad: https://twitter.com/MarkkuPeltonen/status/126113845423635251...
In terms of economy, Sweden's GDP is expected to fall about as much as rest of the EU (~7%).
UK was just one example. Sweden is no worse off that other European countries. You can cherry pick the neighbors but that's doing a disservice.
Of course their GDP is expected to fall. All of the countries are tightly linked together in their economic outcomes.
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.
https://coronavirus.1point3acres.com/en/test
A declining number of hospital beds used is an extremely good sign, but there is very limited data for this nationwide.
The testing is nice to have, but shouldn't really alter people's behavior.
We should instead be teaching people to recognize early symptoms so they can immediately isolate during the time-bounded phase of virus shedding.
Testing is sanitation theater with the side effect of creating a surveillance society.
It's also not the interval immediately after infection takes place (your hour later) that matters, it's the period starting a few days later. Get them out of circulation before they have a chance to spread the virus and we can slow it down further than we have till now, even with more activity taking place.
If the goal is to find a cure before we lift lockdowns we better do something to help those economically impacted by them (and giving away free money is not a viable option). If the goal is to not overwhelm our healthcare systems we are doing that great but a country wide lockdown is not viable either. The New York Times has a good map [0] to show how little most of the country has been affected. That is why state governments should be handling the outbreaks in their own state instead of shutting down the country all together.
These lockdowns were implemented because we had no idea how this virus worked or where it was. We have a much better idea now and each state can act accordingly.
[0]: https://www.nytimes.com/interactive/2020/us/coronavirus-us-c...
[0]: https://www.npr.org/847415273#georgia
edit: April 24 was earlier than May 1 for some lifted restrictions.
https://twitter.com/GAFollowers/status/1261688916375212037?s...
That being said, the messaging hasn’t been calibrated very well.
Everyone talks about the post 9/11 “security theater” of the TSA, but because we’re unable to reasonably assess the threat, today we’ve got equivalent public health theater, but the TSA is us.
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.
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.
"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...
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.
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.
> 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%),
https://en.wikipedia.org/wiki/Common_cold#Viruses
But I've read that most common cold immunities last only for a handful of months or years, not decades.
https://twitter.com/profshanecrotty/status/12610523537733632...
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.
New york did a similar mistake by forcing nursing homes to accept recovering COVID patients, with disastrous results too.
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.