Why Some People Got Sicker with COVID than Others?

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Why are some individuals more adversely impacted by infections, especially Covid? This issue has stumped scientists, but they believe they have found an answer: autoantibodies.

Not only might they explain our susceptibility to infection, but also illnesses like rheumatoid arthritis and diabetes, as well as aging and even prolonged Covid.

Proteins that assault us from inside’ seems more like a plotline for a new science fiction film than a genuine danger to humanity. Autoantibodies, commonly known as “rogue” antibodies, are just that.

They are immune cells that target healthy tissues and crucial organs rather than protecting our bodies against infection.

This mechanism is at the root of a slew of autoimmune illnesses, including rheumatoid arthritis.

In each instance, the immune system misfires, mistaking a body component for foreign and releasing autoantibodies to go ‘on the attack,’ resulting in joint inflammation in rheumatoid arthritis.

Autoantibodies Also Produced by a Healthy Immune System

Until around 20 years ago, it was assumed that they eliminated them, but scientists have now found that autoantibodies persist in certain persons in low concentrations.

However, their number grows as we age, and they play a part in the aging process.

Immunologists are now especially interested in the function of autoantibodies in Covid-19 and extended Covid.

Dr. Jean-Laurent Casanova, a specialist in human genetics and infectious illnesses, and his colleagues at Rockefeller University in the United States have been examining the variables that enhance the chance of having severe Covid-19 as part of an international effort.

They discovered that individuals hospitalized with it had much greater levels of autoantibodies than unaffected patients, and they estimate that autoantibodies may contribute to up to a fifth of all Covid-19 fatalities.

They discovered that autoantibodies aggravated infection by inhibiting the action of molecules that aid in the fight against viral infections.

They also think that low levels of autoantibodies may help explain why some patients have no – or just moderate – Covid symptoms.

Other recent investigations have discovered a variety of autoantibodies in the blood of patients with severe Covid-19 that cause injury in various ways, including targeting proteins that assist in regulating blood clotting.

Because autoantibodies may be discovered in blood tests, screening might help identify persons with high levels who may need preventative therapy — or identify infected patients who require immediate urgent treatment.

Professor Adrian Liston, a senior group leader at the Babraham Institute in the United Kingdom, directs a research program to understand the changes that occur in the immune systems of Covid-19 patients.

While it is too early to establish if autoantibodies have a role in acute or chronic illness, their existence warrants consideration, according to him.

He adds that it is clearly a very realistic approach since scientists have evidence that autoantibodies may remain for years or decades, unlike viruses. Hence, it gives a solid explanation for why long Covid-19 symptoms continue after the virus is gone.

Unprobed Secondary Theory

However, another possibility is that the virus may launch an inflammatory circuit, where inflammation spawns inflammation, and breeds more inflammation long after the infection is gone. Still, experts don’t have enough evidence to tell for sure.

However, it is anticipated that such a study would pave the road for advancements in diagnoses and treatment.
Professor Liston anticipates that a diagnostic tool for long Covid based on autoantibodies will be available within the next six months, followed by therapy.

While Covid has undoubtedly increased interest in autoantibodies, they were already the topic of significant study before the pandemic, partly because of worries about the alarming rise in autoimmune illnesses.

There are four million people in the UK who have at least one autoimmune condition. Still, according to Dr. Louisa James, a senior lecturer in immunology at the Queen Mary University of London, the prevalence is expected to rise partly because there are probably more syndromes and conditions out there where our immune system is playing a previously unrecognized role.

According to her, recent research discovered that fibromyalgia, which causes widespread pain, maybe an autoimmune illness caused by antibodies that impair pain sensitivity.

Paul Morgan, a Cardiff University professor of immunology, is optimistic about the future of autoantibody research and believes that using information from the study of autoimmune illness might lead to novel therapies for Covid-19 and extended Covid.

If autoantibodies are actually responsible for many of the symptoms of extended Covid, then you might treat it using the same treatments that have been discovered for autoimmune disorders – medications that lower the quantities of dangerous antibodies.

That’s why it’s significant; it might lead to a method of really treating the illness – by targeting autoantibodies.

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