New research from CSHL scientists suggests that tobacco smoke spurs the lungs to make more ACE2 (angiotensin-converting enzyme 2), the protein that the novel coronavirus which is responsible for COVID-19 grabs and uses to enter human cells. The findings of the study are published in the journal Developmental Cell, explains why smokers are likely to be particularly vulnerable to severe respiratory infections. The analysis indicates that the change is reversible, proposing that quitting smoking may lessen the risk of COVID-19 infection.
From the early stages of the current coronavirus pandemic, researchers and clinicians have observed dramatic differences in how individuals respond to coronavirus infection. Most infected people have an only mild illness if they experience any at all. But others may require intensive care or ventilator. Three gatherings, specifically, have been altogether almost certain than others to develop serious ailment: men, the old, and smokers.
With most laboratory experiments on hold due to the pandemic, CSHL Fellow Jason Sheltzer and Joan Smith, who is an engineer at Google, turned to recently published data to look for possible explanations for these variations. They were curious to know whether the vulnerable groups may share some key feature related to the human proteins that the novel coronavirus relies on for causing the COVID-19 disease.
They started gathering all the possible data they could find and focused first on comparing the gene activity in the lungs between the sexes, across different age groups and between smokers and nonsmokers. When they put it all together and started analyzing it, they observed that both mice that had been exposed to smoke in a lab and humans who were current smokers had significant up-regulation of ACE2.
Sheltzer shared that no evidence related to the age or sex was found as it may impact the levels of ACE2 protein in the lungs, the effect of smoke exposure was quite strong. The difference appears to be temporary but the data revealed that the level of ACE2 proteins in the lungs of individuals who had stopped smoking was surprisingly similar to that of non-smokers.
Sheltzer, Smith, and their colleagues also found that the most prolific producers of ACE2 protein in the airways are mucus-producing cells which are known as the goblet cells. Smoking increases the prevalence of such cells, a change that can protect the airways from irritants but by increasing the levels of ACE2 proteins in the lungs can also increase vulnerability to SARS-CoV-2 and risk of COVID-19.
Cigarettes appear to be an unlikely ally against the coronavirus. Tobacco smoke damages the minuscule air sacs in the lungs where oxygen enters the blood and hinders the hairs lining the air passages of the body that gently float along with the mucus. Smokers are more severely affected by flu and colds, and a long period of smoking may lead to the type of lung failure called emphysema, which is the type of chronic obstructive pulmonary disease.
But data from the countries first hit by the novel coronavirus gave doctors stop, the extent of smokers among those being hospitalized for COVID-19 was lower than in non-smokers. For example, in China, about 8 per cent of infected individuals in the hospital were smokers, while 26 per cent of the general population smokes. The same figures for Italy are 8 and 19 per cent respectively.
Alberto Nájera at the University of Castilla-La Mancha in Spain, whose team analysed figures from 18 of the first such reports, said that the data seem to be repeated in different countries. He says nicotine may reduce the tendency of the immune system to overreact to the novel coronavirus and cause the cytokine storm, the inflammatory response that can be fatal.