Recently published research suggests Covid-19 is more than a lung disease.
SARS-CoV-2, which causes Covid-19, appears to infects an individual via an enzyme known as ACE2 (angiotensin converting enzyme 2). SARS-CoV-2 prefers to infect and latch on to cells that have ACE2 on the outside.
ACE2 is found in endothelial cells, which line the interior surface of blood vessels and lymphatic vessels and in the lung, kidney, intestine and heart.
Research published on 20 April 2020 in The Lancet based on post mortem analysis of Covid-19 patients found evidence of endothelial and inflammatory cell death in a number of these organs.
Earlier Italian research suggests those with an ACE2 deficiency in the parts of the body where ACE2 is present are more likely to suffer the worst effects of Covid-19. It is possible that ACE2 deficiency amplifies inflammatory and hyper-coagulation processes. ACE2 down-regulation induced by SARS-CoV-2 invasion may be especially detrimental in people with baseline ACE2 deficiency, said the authors.
ACE2 deficiency and endothelial cell dysfunction both appear to be associated with smoking, hypertension, diabetes, obesity, and cardiovascular disease.
These two research results together might help to further explain clinical data on Covid-19 deaths. Patients with hypertension, diabetes, obesity, and cardiovascular disease are more likely to die from the virus.
In addition, these conditions are more prevalent among men, who have suffered disproportionately from Covid-19.
More on this:
The Lancet report (in English)
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