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There have been indications that smokers and people in India and possibly (?) China are less likely to suffer serious syptoms from corona virus.

Although several explanations are possible, and the statistics may well be faulty either by accident or design, taking these facts at face value one thing common to both is elevated CO levels, from the tobacco smoke and from traffic and wood fire pollution.

It isn't commonly known, but the body uses CO for various purposes such as part of its nerve signalling mechanism. See https://en.wikipedia.org/wiki/Carbon_monoxide :

Carbon monoxide is produced naturally by the human body as a signaling molecule. Thus, carbon monoxide may have a physiological role in the body, such as a neurotransmitter or a blood vessel relaxant.[40] Because of carbon monoxide's role in the body, abnormalities in its metabolism have been linked to a variety of diseases, including neurodegenerations, hypertension, heart failure, ..

The natural role of CO in the body (aside from its toxic effects) was discovered only in 1993, and is still an active area of research with many unknowns.

Now some Covid symptoms, such as loss of taste and smell (as seen to some extent in smokers), and often a general feeling of muddle headedness for some time during recovery are similar to symptoms and chronic after effects of CO poisoning, e.g. https://www.st-va.ncbi.nlm.nih.gov/pmc/articles/PMC3850907/

A possible implication of this is that the CV virus somehow prompts the body to produce excess CO, to a toxic extent. So my question as in the title is whether (1) This is a likely explanation and (2) If so, could its effects be ameliorated in advance by building up a small degree of CO tolerance under controlled conditions?

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    Two things: first, where are you seeing these indications that smokers are less likely to suffer serious symptoms? Everything I've seen says exactly the opposite. And second, read up on "flu-like symptoms": since this particular collection of symptoms is caused by immune system activation rather than by the disease agent, they can be triggered by anything from a rhinovirus infection to opioid withdrawal. – Mark May 2 at 1:16
  • This question would be improved by adding a link to support the claims in the first paragraph. – Carey Gregory May 2 at 5:05
  • I wasn't planning to return to this question when I noticed some anonymous cowardly dog had marked it down without giving a reason! But glad I did take a last look, and very many thanks to those who have commented and answered. The French study I referred to at the start is mentioned at nytimes.com/reuters/2020/04/27/world/europe/… . I guess tests of whether nicotine chewing gum or vapes have the same supposed (?) beneficial effects as tobacco smoke will determine whether nicotine is indeed the relevant ingredient. – John Ramsden May 2 at 13:37
  • @JohnRamsden People downvoting without explanation is extremely common across all SE sites. I recommend getting used to it and not letting it get to you. If you get multiple downvotes then that's meaningful and it says you need to review your question and fix what's wrong, but if it's only a single downvote then just ignore it. – Carey Gregory May 2 at 21:45
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There are a couple of theories to explain why smokers appear to be under represented in severe cases of COVID-19.

  1. Smoke appears to upregulate the expression of ACE2 receptors in the lung. We have both animal experiments that show that mice exposed to smoke increased the numbers of ACE2 receptors. More ACE2 receptors is thought to help prevent lung damage.

The team inspected tissue samples from mice that had been exposed to diluted cigarette smoke for zero, 2, 3 or 4 hours a day over the course of five months. They found that, the more smoke exposure, the more ACE2 receptors studded the animals' lungs. Compared with unexposed mice, the mice that received the highest dose of cigarette smoke accumulated about 80% more ACE2 receptors in their lungs. The researchers then compared the lungs of human smokers against those who never smoked, and again, they found a similar trend: Smokers’ lungs contained 40% to 50% more ACE2 receptors than those of nonsmokers.

  1. Nicotine may bind to ACE2 receptors blocking the virus's infection of cells

  2. Nicotine may have an anti-inflammatory effect. It is known that cigarette smoking cessation is linked to the onset of ulcerative colitis. It may involve the nicotinic acetylcholine receptor (nAChR)

A potential protective effect of smoking and of nicotine on SARS-CoV-2 infection has been noted. Until recently [39], no firm conclusions could be drawn from studies evaluating the rates of current smokers in Covid-19. All these studies [40-48], although reporting low rates of current smokers, ranging from 1.4% to 12.5%, did not take into account the main potential confounders of smoking including age and sex. In the study that two of us are reporting [1], the rates of current smoking remain below 5 % even when main confounders for tobacco consumption, i.e. age and sex, in- or outpatient status, were considered. Compared to the French general population, the Covid-19 population exhibited a significantly weaker current daily smoker rate by 80.3 % for outpatients and by 75.4 % for inpatients. Thus, current smoking status appears to be a protective factor against the infection by SARS-CoV-2.

I have not seen any data to suggest carbon monoxide is important in the pathogenesis of COVID-19.

A nicotinic hypothesis for Covid-19 with preventive and therapeutic implications. https://www.qeios.com/read/FXGQSB.2

https://www.euronews.com/2020/04/28/covid-19-and-smoking-what-does-the-who-say

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