قالب وردپرس درنا توس
Home / Health / Coronavirus: Some survivors will form destructive “autoantibodies”

Coronavirus: Some survivors will form destructive “autoantibodies”



New research shows that coronavirus survivors develop immune cells that fight infection, and may turn on some of them and attack healthy tissues.

Scientists at Emory University suspect that off-target attacks by these rogue immune cells may be the culprit for the lingering symptoms of COVID-19 “long-distance travelers”.

The so-called “autoantibodies” are similar to the autoimmune response seen in diseases such as lupus, certain forms of hepatitis and rheumatoid arthritis.

If the autoantibody of the coronavirus meets these conditions, a long-term cure may not be cured.

But now, scientists have discovered that they can test these rogue antibodies. They hope they can identify who has these rogue antibodies and develop treatments to fight sudden onsets, just like those for earlier autoimmune diseases.

More and more coronavirus survivors report symptoms that still exist months after the virus is cleared. Researchers at Emory University believe that this may be due to the

More and more coronavirus survivors report symptoms that still exist months after the virus is cleared. Researchers at Emory University believe that this may be due to the “autoantibodies” produced by the human body to fight the coronavirus, but against healthy tissues (document)

The number of coronavirus survivors suffering “long-term symbiosis” is difficult to determine, but it is still increasing.

A study found that among COVID-19 patients hospitalized in the UK due to infection, 81 of 110 patients (about 74%) still showed lingering symptoms three months after being discharged from the hospital.

Other studies estimate that this number is closer to a very conservative figure.

The lingering symptoms have affected people of all ages, including children and adolescents as well as the elderly and pregnant women.

Several months after the virus is cleared, some people will have periodic breathing difficulties.

Others suffer from draining fatigue, rash or diarrhea.

The team of researchers has been searching for answers to find out why some people (many of whom were in good health before contracting the coronavirus) become “long-distance travelers”, while others become over-infected within days or weeks No symptoms.

Underlying chronic diseases seem to be more common in severely ill patients, but this also makes people question why these people are so sicker than others.

A recent study found that out of 110 patients 12 weeks after being discharged from a British hospital, 81 still had symptoms such as dyspnea, fatigue, loss of smell and muscle aches.

A recent study found that after 12 weeks from a hospital in the UK, 81 of 110 patients still had symptoms of breathing difficulties, excessive fatigue, loss of smell and muscle pain.

Some scientists have cited genetics as a possible explanation, but the immune overreaction that Emory’s team saw during the course of COVID-19, the pattern of “flare attacks” is similar to other non-infectious manifestations A connection is established between diseases.

They also noticed that certain immune proteins and cells in the blood of COVID-19 patients suggest that the antibody attack is in the wrong direction.

Antibodies are immune proteins produced by B cells. They are tailored after the human body recognizes new bacteria or viruses (such as SARS-CoV-2). Some genetic codes from pathogens become instructions for B cells to start producing customized weapons.

But sometimes, this system becomes chaotic, mistakes certain parts of the human genetic code as targets, and designs weapons to find and destroy these weapons.

These are called “autoantibodies”-anti-autoantibodies made by the human immune system.

Dr. Marion Popper, an immunologist at the University of Washington in Seattle, said: “Whenever inflammation and cell death coexist, autoimmune diseases and autoantibodies are more likely to occur.”

To test their theory, Emory’s team performed a series of blood tests on 52 coronavirus patients who were discharged from the hospital with “severe” or “severe” illnesses in Atlanta, Georgia.

In 44% of the entire research team, they found autoantibodies that reacted to fragments of human DNA.

In half of the patients with the disease, more than 70% of the patients have these self-destructive immune cells, and many patients also have antibodies that neutralize the protein, which plays a vital role in the formation of healthy blood clots. It is called rheumatoid factor.

These deformed autoimmune weapons can well explain the inflammation and cardiovascular problems seen by many long-distance transporters.

A few months later, it has been proven that the precisely formed anti-coronavirus antibodies will weaken, which may mean that the protection against reinfection is indeed the same.

What remains to be seen is whether autoantibodies will dissipate over time-or continue for years, leading to the development of chronic diseases, like lupus or rheumatoid arthritis.

In the latter case, being able to test these autoantibodies may be the first step in designing treatments that can inhibit their effects.

However, if this phenomenon follows the pattern of other autoimmune diseases, it cannot be cured.

‘You have never really cured lupus- [patients] Dr. Ann Marshak-Rothstein, an immunologist at the University of Massachusetts at Worcester, told The Times.

“This may be related to autoantibody memory.”


Source link