Smokers have a hard time COVID-19 – there is a lot of evidence for this, and the reasons for this are more or less well known. For example, we wrote about a study by employees of the University of California at Los Angeles: they found that due to tobacco smoke, cells decrease the activity of interferons – signaling immune proteins that play an extremely important role in antiviral immunity.
But not everything is so simple. There is evidence that smokers are less likely to catch the new coronavirus. Why this can happen is explained in Scientific Reports researchers from Hiroshima University… In tobacco smoke, there are so-called polycyclic aromatic hydrocarbons, or PAHs, that interact with Ah receptors (AHRs). Ah receptors control the activity of many different genes: having sensed PAHs, they transmit a signal into the cell nucleus, forcing certain genes to work more intensively.
First of all, Ah-receptors activate those genes that are needed to destroy xenobiotics, the very PAHs. But now researchers have found that Ah receptors also affect the gene encoding another receptor, ACE2. Recently, ACE2 has become extremely famous even in not very scientific circles: the fact is that the SARS-CoV-2 coronavirus, in order to enter the cell, must interact with ACE2. That is, the more ACE2 receptor on the cell, the more chances it has to become infected with coronavirus. At the same time, the activity of the gene ACE2 depends on the activity of another gene, CYP1A1: the more active CYP1A1, the less active ACE2… And the Ah receptors just stimulate the activity of the gene CYP1A1.
In the experiments, cells of the epithelium of the oral cavity, lungs and liver were used – they synthesize especially a lot of ACE2. They were treated with an extract with substances from cigarette smoke during the day. The more extract there was, the more active the gene was in the cells of the lungs and liver CYP1A1, and the less they had an ACE2 receptor. (The cigarette smoke extract had the same effect on the cells of the oral cavity, but weaker.) And the smaller the ACE2 receptor, the less the virus has a chance to enter the cell.
Researchers managed to find a substance that would mimic this effect of smoke – this is 6-formylindolo[3,2 – b]carbazole (or FICZ), which is derived from the amino acid tryptophan, and omeprazole, a drug that suppresses gastric acid secretion. Both FICZ and omeprazole attenuated the synthesis of the “coronavirus” ACE2 receptor via Ah receptors.
It does not follow from this that you need to immediately start drinking omeprazole to protect yourself from the coronavirus. Experiments were performed with cell cultures growing in a nutrient medium under laboratory conditions. The big question remains, how does this all happen in humans. The fact is that there is data on the level of the ACE2 receptor in smokers and nonsmokers that directly contradict the above results. Last year, we talked about a study published in European Respiratory Journal – it said that the lung cells of smokers contain more ACE2 protein than non-smokers. Maybe here it is necessary to take into account the smoking experience and the intensity, but, one way or another, the cellular results remain cellular, and it is better to postpone it with practical recommendations.
Source: Автономная некоммерческая организация "Редакция журнала «Наука и жизнь»" by www.nkj.ru.
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