They learned that smoking opens more doors for the virus in the lungs

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Substances in cigarette smoke stimulate the production of an enzyme that facilitates the copying of SARS-2

The good news: for people who have quit smoking, the level is close to that of non-smokers

Despite the daily replenishment of the risk groups for the new coronavirus disease, three remain unshakable and most numerous.

Until resuscitation

get more

the adults,

men and smokers

These data, first exported from China, are later confirmed in all countries that the virus has invaded.

Attempts to challenge seem to be caused only by smoking, but the emerging operational data from hospitals do not give reason for doubt.

A new publication from the Cold Spring Harbor Research Laboratory in New York claims that smoking alters the lungs in a way that makes it easier for the coronavirus to bind to lung cells.

Scientists also have a theory as to why this is so: substances in cigarette smoke stimulate the lungs to produce more than a key enzyme with a role in the virus’s penetration into the lower respiratory tract.

The virus responsible for COVID

used for

entering the cells

of the lungs

ACE2 protein

(angiotensin-converting enzyme 2), with which they are seeded. Although they found no evidence that age or gender increased ACE2, researchers found experimentally that exposure to smoke had a surprisingly strong effect. In the May issue of the medical journal Cell Development, they explain why smokers appear to be particularly vulnerable to severe COVID infections.

Since the early stages of the pandemic, scientists and clinicians have noted dramatic differences in the way people respond to infection with SARS-CoV-2, a virus so genetically close to a family’s previous one that it was expected to behave similarly, but it doesn’t happen. .

Most infected people suffer from only a mild illness, if they have any flu-like or gastrointestinal symptoms. It is estimated that this is between 70 and 80 percent of those infected with the coronavirus. But the condition of others requires treatment, some – intensive care, inclusion in mechanical respiration, and yet the effort does not always end in success.

Scientific curiosity and the search for successful treatments are leading researchers around the world to examine whether vulnerable groups share any key characteristics related to the human enzymes that the coronavirus relies on to enter the lungs. The living cell is his only chance to copy and he is looking for ways to capture it.

The most prolific producers of ACE2 in the respiratory tract are

cells called

goblets that

synthesize mucus

It has long been known that in order to respond to respiratory irritation from smoking, the body increases the number of mucus-producing cells. But proportionally, the amount of ACE2 in the lungs increases, which increases the vulnerability to SARS-CoV-2 or SARS-2, as the new coronavirus came to be called for short.

Scientists compare

genetic activity

in the lungs

through different

periods of time, make comparisons between the sexes and between smokers, non-smokers throughout their lives and quit smoking. When they collected all the data from animal and human studies and analyzed them, they saw that both mice that had been exposed to smoke in the laboratory and people who were currently smoking had a significant increase in ACE2. This is another argument that can arouse the attention of smokers who fall asleep vigilant about the infection, hoping to be protected from nicotine.

The good news is that marking extra “loopholes” seems temporary: the level of the enzyme in the lungs of people who have given up smoking is similar to that of non-smokers.





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