re: Coronavirus Disease 2019 (COVID-19) ***W.H.O. DECLARES A GLOBAL PANDEMIC***

Cliffs Notes (Spark Notes) on Actrema?

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there is a running hypothesis right now that those with somewhat recent MMR vaccination history are faring better.

There is a spike protein on the Rubella portion of the MMR attenuation that is 30%~ similar to the SARS2CoV19 virus.

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If true shouldn’t healthcare workers fair better? We all have to get updated MMR boosters when our bloodwork shows we need them

Wouldnt people who had the measles have the same immunity as if they'd been vaccinated? Before the mmr vaccine (which came about in the sixties IIRC) most people got measles as a child. Seems like they would also be protected, but fhat demographic is the hardest hit.

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It’s also worth mentioning there were some nasty measles outbreaks in the 90s in Italy because they didn’t like getting vaccinated. That population would be a little older now and more vulnerable...

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What do we know about the UK's history with the vaccination?

The UK is well on their way to faring much worse than Italy in this.

Been on a strong iu vitamin d for years. When I got Corona I got pretty bad but even as a twenty year smoker and ex drug addict all I needed was nasal oxygen hydroxychloroquine to make a complete recovery in two weeks. One year my entire family got the flu and struggled yet I was able to function at a much higher level. My doctor is the one that put me on it.

Hey Tiguar, on the topic of the coefficient of variation in susceptibility to infection, the evidence continues to pile up that smokers are lot less susceptible. A new preprint:

"in the Chinese population, the prevalence of smokers among COVID-19 patients has been reported between 1.4% and 12.6% (2-4), and also the very recent data coming from the New York City outbreak confirm a low prevalence of smokers in COVID-19 patients, in this case at 5.1%.
These prevalence figures are so much lower than the respective national smoking rates (in China 24.7%, and in US 17.25%) that suggest it is worth to further investigate whether there is an inverse association between smoke and predisposition to SARS-CoV-2 infection."

"Italy is the European Country with the highest number of deaths from COVID-19. Based on the sources of data used in this study, 441 COVID-19 patients were admitted between 5 and 31 March 2020. Active smokers were only 21, this number corresponding to less than 5% prevalence of active smokers, which is disproportionately low compared with the 24% prevalence of smokers in the general Italian population."

So, smokers would seem to be between 3 and 5 times less likely to be infected that nonsmokers.

I've seen the hypothesis that nicotine binds to cells in the same places that the virus does, and so nicotine might block the virus from entering the cell. I know that they started a study in France back on April 22nd, experimenting with nicotine patches to see if they have an effect.


But, anyway, I'm going to quote from the post I made on the previous page:

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I didn't consider the possibility that stronger immune systems or other factors may simply prevent infection at lower levels of viral load. If some people get sick at a given level of exposure and others don't, then again, the virus has already gotten much of the low-lying fruit, so to speak. And there's a lot of reason to think that this is the case; we know that children, for example, seem to be less likely to become infected.

What this means is that there could be true herd immunity with as little as 20% of the population having antibodies. We really don't know, because we don't know just variable people are (the authors state that research here should be a priority).

The fact that hospitalizations in Sweden have peaked and are headed downward indicate that there might be some truth in the hypothesis, advanced in this paper, that a coefficient of variation of infection for this virus might be about 3, which would support the idea that places like Sweden and NYC might already have reached herd immunity.

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The more that I think about it, the more likely it seems to me that the authors of that paper are correct in their hypothesis that the coefficient of variation might be about 3, which would mean that herd immunity could be achieved with as little as 20% of the population having antibodies.

There's just no other reason right now for Sweden's hospitalization numbers to be decreasing. They haven't enacted any new significant social-distancing restrictions. I suppose it's possible that people have voluntarily decided to restrict social interaction more as fatalities have piled up, but this seems very unlikely from all the reports that I read from there. Their R value should still be above 1, and it isn't.

I was very much against any kind of a herd immunity strategy when it was believed that it would take 60-70% of the population getting the virus to achieve it. If we can get herd immunity at 20%, though, I'm very much of the opinion that we can open everything up, have people wear masks for a while, and eliminate big events that create opportunities for superspreaders -- and we'll be just fine. COVID-19 is going to go away this summer.

We certainly need some data from serologic studies to know whether fewer smokers in the hospital is primarily due to an effect of nicotine in preventing infection or whether it helps attenuate cytokine storms.

Here's the study that references French smokers and their low rate of hospitalization, and which provides the basis of the nicotine patch study. LINK

These authors have what would seem to me to be a rather speculative hypothesis, but they seem convinced that nicotine prevents infection.

What I would like to see is an update to this VA study that was published April 14th.

It found that black veterans were four times as likely as white veterans to test positive for COVID-19. The authors note that while there are significant differences between the quality of health care that black and white Americans receive, those differences are much smaller among veterans (who are all presumably going to get the same quality of care at the VA). That held true when controlling for location tested (New Orleans vs New York made no difference).

Simply put, you can't explain why black veterans were 4 times likely to test positive (more likely to seek testing and more likely to receive a positive result) by looking at comorbidities or by quality of health care. The only reasonable explanation is Vitamin D.

This study also showed smokers who were tested were half as likely as nonsmokers to test positive. What was interesting is that, among those who tested positive, the smokers were slightly more likely to be hospitalized and be in an ICU, although the sample is too small for this to be significant.

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Been on a strong iu vitamin d for years.

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Do you have your levels checked?

Even with supplementation if your magnesium is low or because of other factors you can still have low Vitamin D

Also the idea is not that you wouldn’t get a bad cold, you just would be less likely to go into a cytokine storm. But that’s just the hypothesis backed by some data, far from proven fact.

I think I found it.

Yeah, if having caught a "common-cold" coronavirus in the last two years offered protection from COVID-19, that would introduce a tremendous amount of variation of infection.

And all this discussion is before we even get into the variables of viral load and transmissibility! We obviously know that some people get sicker than others from COVID-19, and those people have a higher viral load of the SARS-coV-2 virus. That likely means that they transmit the virus to more people than those who have mild or asymptomatic cases.

Again, if we assume that those who are most susceptible to the virus are the low-hanging fruit that the virus has already infected, the R value of COVID-19 drops even absent other factors, because the people getting the virus later on transmit it to fewer people than those who got it earlier in the lifecycle of the pandemic.