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'Rebel' antibodies, responsible for severe forms of Covid-19?

'Rebel' antibodies, responsible for severe forms of Covid-19?

More than a year after the pandemic began, there are still many unresolved questions about Covid-19. Why do some people get sick more than others? What is the mechanism at the origin of the systemic condition that afflicts those suffering from "Long Covid"?

According to the latest studies, at least some of these issues can be explained by autoimmune mechanisms, phenomena in which antibodies, instead of attacking external pathogens, attack the human body itself. An overactive immune response - the famous cytokine storm, the protein that regulates the human body's defense mechanisms - was mentioned early in the pandemic.

But another side of the coin of autoimmune mechanisms, has to do with the less in-depth role of autoantibodies, antibodies that get out of control and attack certain components of our immune system or attack specific proteins in certain organs, starting with heart.

If the damage from the ‘cytokine storm’ is systemic and acute, that of autoantibodies targets specific tissues and lasts longer over time. Even healthy people can produce autoantibodies, but usually not in harmful amounts to the body. But in some cases, they can play a role in the progression of various infections, including Covodi-19.

As explained in a lengthy article in the journal Nature, some people may be more prone to produce autoantibodies that can get out of control during infection. A study published in the journal Science by Rockefeller University in New York found that over 10 percent of the 987 patients affected by severe pneumonia due to Covid-19 had autoantibodies targeting type 1 interferons, molecules that enhance the immune response to external pathogens.

This finding is interesting, as these autoantibodies, which in some people are present even before coronavirus infection, are rare in the general population, and were virtually absent in the control group. According to the study authors, this is probably why some people, even very young ones, become seriously ill with Covid-19.

These autoantibodies appear to be more common in men, who are more likely to have more severe forms of coronavirus infection. Now the same study group led by Jean Loren Kasanova is observing 40,000 patients to better understand the link between the presence of pre-existing autoantibodies, age, gender, ethnic origin and the frequency of the severe form of Covid-19.

Dëshmia e parë shkencore se ekzistojnë autoantitrupa të aftë për të penguar aktivitetin e interferoneve, dhe se ato mund të shkaktojnë një rrezik më të madh nga infeksionet, daton nga mesi i viteve 1980, por pandemia e ka risjellë në vëmendje këtë çështje.

Por a mund të ndodhë që SARS-CoV-2 të stimulojë prodhimin e autoantitrupave të dëmshëm? Një studimi nga një grup tjetër kërkimor, i udhëhequr nga shkencëtarët e Shkollës së Mjekësisë të Universitetit të Jeilit në SHBA, sugjeron se po. Pas testimit mbi praninë e llojeve të ndryshme të autoantitrupave tek 194 pacientë të prekur nga Covid-19 me ashpërsi të llojeve si dhe tëstafit spitalor, shkencëtarët arritën në përfundimin se njerëzit e infektuar kishin një prevalencë më të lartë të autoantitrupave sesa ata që nuk ishin infektuar.

Some antibodies attacked B lymphocytes, others interferons. In some of the Covid-19-positive patients, these autoantibodies appeared to target the blood vessels, heart and brain, organs and tissues that were most damaged by the virus attack.

Another study, published last November, found anti-phospholipid-directed autoantibodies in 52 percent of the 172 people hospitalized with Covid-19. Some phospholipids play an important role in controlling blood clotting, a function that is out of the question in those affected by severe forms of Covid-19.

* Received from Bota.al