CO耐性はある程度まで可能であり、COVID-19症状を改善する可能性がありますか?


1

インド、そしておそらく(?)中国では、喫煙者と喫煙者がコロナウイルスによる深刻な症状に苦しむ可能性が低いという指摘がありました。

いくつかの説明が可能であり、統計は偶然または設計のいずれかによって誤っている可能性がありますが、これらの事実を額面どおりに見ると、両方に共通する1つのことは、タバコの煙や交通や薪火による汚染からのCOレベルの上昇です。

これは一般的には知られていませんが、身体はCOを神経信号伝達メカニズムの一部などのさまざまな目的に使用しています。https://en.wikipedia.org/wiki/Carbon_monoxideを参照してください。

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, ..

体内でのCOの自然な役割(その毒性効果は別として)は1993年にのみ発見され、未だ多くの未知数を伴う活発な研究分野です。

さて、味覚や匂いの喪失(ある程度は喫煙者に見られる)などのいくつかのCovid症状と、回復中のしばらくの間のだらだらした頭痛の一般的な感覚は、CO中毒の影響と慢性の症状に似ています。例えばhttps://www.st-va.ncbi.nlm.nih.gov/pmc/articles/PMC3850907/

これの可能性のある含意は、CVウイルスが何らかの形で過剰なCOの生成を毒性のある範囲で促すことです。タイトルと同じように私の質問は、(1)これはありそうな説明であり、(2)そうであれば、制御された条件下で少しのCO耐性を構築することによって、その効果を事前に改善できますか?

2

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