Scientists discover that smokers are in danger of getting intubated, because of the lungs producing ACE2 (angiotensin-converting enzyme 2) which helps the coronavirus infect the lungs more efficiently.
Cold Spring Harbor Laboratory scientists conducted a study on COVID-19 and found out these alarming findings in the course of their studies that shed light on something relevant for all smokers. This study might explain why smokers are getting the worst symptoms when infected by the coronavirus.
Vital role of ACE-2 in infecting smoker's lung
Why does the ACE-2 seem to be a factor for causing a worse coronavirus infection in smokers? First off, the ACE-2 is the coronaviruses ticket to enter host cells, in this case, it is human cells.
When the virus finds its way into the body, the coronavirus is searching for ACE-2 enzymes covering the lung tissue, and this where the infection begins in full.
A study posted on May 16, 2020, postulates why a smoker is so weak when struck by severe infections, like the coronavirus. Though some evidence does point to a chance that ACE-2 might not compromise smokers.
Turning your back on smoking may prevent any coronavirus case that might become a severe case, in which you end up getting intubated. This ends fatally for some patients.
One observation about the coronavirus is to what extent will the ACE-2 be there in the surrounding tissue.
How severe are the symptoms from patient to patient
The severity of symptoms will vary according to the patient, and most scientists and doctors have observed differences in how they react to getting infected with the coronavirus. For example, some will experience milder symptoms. Some who were unlucky enough will need intensive care when the infection goes full throttle to go fatal, or just barely survive the viral attack.
Health professionals will be looking out for these particular groups, which have a greater chance to progress into severe or fatal viral attacks. These particular groups include men, elderly, and smokers.
With the pandemic causing widescale lockdowns and stay at home orders, several CSHL scientists used information from or other studies to analyze the problems associated with it. They are looking for clues that are related to human physiology that will provide a lock on point for the coronavirus to infect the host cells.
ACE-2 as an enabler in smokers and non-smokers
Sources were examined to find somewhere to start forming an idea to begin from. A comparison was then done on genetic activity of the lung from several age groups, sexes, soon after smokers and non-smokers. Once all the links were examined, what stood out are mice exposed to smoke with humans as well. They found out later there was more ACE-2 produced for those exposed to smoke.
Some results point to no connection to age or sex that will produce more ACE-2, but inhalation of smoke increases the ACE-2 proteins. Further indicators show non-smokers and people who just quit smoking, the same ACE-2 levels.
They also found out that ACE-2 was produced in the airways by goblet cells which secret mucus. Smokers have increased ACE-2, and make it easy to get infected by the coronavirus, and maybe get intubated too.