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The coronavirus can distort the body’s defenses in several ways – disarming the body’s early warning systems, for example, or causing immune cells to misfire. But a slew of new studies suggests another insidious consequence: infection can trigger the production of antibodies that mistakenly attack the patient’s own tissues instead of the virus.
The latest report, published online this week, suggests that the so-called autoantibodies may persist for months after the infection resolves, possibly causing irreparable damage. If other studies confirm the finding, it may explain some of the persistent symptoms in people who have recovered from Covid-19. The syndrome, sometimes called Covid long, can include dementia, “brain fog” and joint pain.
Autoantibodies aren’t new to science – they’re the misguided soldiers of the immune system, linked to debilitating diseases like lupus and rheumatoid arthritis, that occur when the body attacks its own tissues.
The latest study is small, with just nine patients, five of whom had autoantibodies for at least seven months. It has not yet been peer reviewed for publication, and the authors called for caution in interpreting the results.
“It’s a signal; it’s not definitive, ”said Dr. Nahid Bhadelia, medical director of the Special Pathogens Unit at Boston Medical Center, who led the study. “We don’t know how widespread it is and whether or not it may or may not be linked to a long Covid.”
The issue of autoimmunity following coronavirus infection is urgent and important, added Dr Bhadelia. Up to one in three Covid-19 survivors report still experiencing symptoms.
“It’s a real phenomenon,” she says. “We are envisioning a second pandemic of people with continuing potential disability who may not be able to return to work, and this is having a huge impact on health systems.”
A growing body of evidence suggests that autoimmunity contributes to the severity of Covid-19 in some people. A study published online in October found that among 52 patients with severe Covid-19, more than 70% carried antibodies against their own DNA and against proteins that help blood clotting.
In another study, also published online in October, researchers found autoantibodies to carbohydrates made by the body in patients with Covid-19, which could explain the neurological symptoms. And a study published in November in the journal Science Translational Medicine found that half of patients hospitalized with Covid-19 had at least transient autoantibodies that cause clots and blockages in blood vessels.
The research collected raises the worrying possibility that persistent autoantibodies could lead to autoimmune disease in some people infected with the coronavirus.
“Once these autoantibodies are induced, there is no going back,” said Akiko Iwasaki, immunologist at Yale University. “They will be an integral part of the person’s immune system.”
She added, “What is he doing about the vaccine response? What does it do with newly acquired infections? These are all questions that will need to be answered. “
Dr Iwasaki’s team showed in December that critically ill patients had dramatic increases in a wide range of autoantibodies that target parts of the immune system, brain cells, connective tissue and coagulation factors.
“We are really seeing largely reactive autoantibody responses in these patients,” said Dr. Iwasaki. She had suspected that autoimmunity might play a role, but “even I didn’t expect to see so much auto-reactivity.”
Dr Iwasaki and her colleagues drew blood from 172 patients with various symptoms, 22 healthcare workers who had been infected and 30 healthcare workers who had not been infected.
One in five infected patients had autoantibodies against five proteins in their own body and up to 80% against at least one protein, the researchers found. Patients with severe Covid-19 had many more of these antibodies, which hampered their immune responses and exacerbated the disease. Of 15 patients who died during the study, 14 had autoantibodies directed against at least one component of the immune system.
The study convincingly shows that autoantibodies “change the course of the disease,” said Marion Pepper, an immunologist at the University of Washington in Seattle who was not involved in the research.
Autoimmunity after illness is not unique to the coronavirus. Other intensely inflammatory infections, including malaria, leprosy, and respiratory viruses, are also known to trigger autoantibodies. But autoimmunity and Covid-19 can be a particularly dangerous mix, experts have said.
An analysis of nearly 170,000 people with rare autoimmune rheumatic diseases like lupus and scleroderma indicated they face increased risks of death from Covid-19. And a study of more than 130,000 people found that autoimmune diseases such as type 1 diabetes, psoriasis and rheumatoid arthritis increase the risk of respiratory complications and death from Covid-19.
Some of the antibodies appeared to be the result of innate defects in the immune system. For example, a study published in the journal Science in October found that about 10% of critically ill Covid-19 patients had existing autoantibodies that attack key components of the immune system believed to be triggered after exposure to the virus. Without this swift response, the body’s defense is hopelessly retarded, waging a losing battle against the multiplying virus.
However, the mere presence of autoantibodies does not indicate damage. They are part of the general population and do not always lead to disease, some experts have noted.
“Anywhere from 10 to 15 percent of the population has some level of this self-reactivity,” said Dr. Iñaki Sanz, immunologist at Emory University. “The problem is, you need a lot of other events downstream from autoantibodies to induce disease.”
At least in some patients, autoantibodies have clearly developed as a result of the disease, Dr. Iwasaki’s study showed. Extreme inflammation caused by viral infections can cause cells to burst, spewing out their contents and disrupting the immune system’s ability to distinguish “self” from “other”.
But autoantibodies induced in this way can stabilize after a few months, said Dr Shiv Pillai, immunologist at Harvard University: “Probably in the vast majority of patients with Covid-19, autoantibodies emerge in the acute phase. , then decrease.
“That being said, yes, it would be interesting if the long Covid could be explained by specific autoantibodies,” he added.
Several researchers, including Dr Bhadelia and Dr Iwasaki, follow patients over time to see how long the autoantibodies persist and if they are causing permanent damage. Although scientists have known that acute infections can trigger their presence, the phenomenon has never been studied in such detail.
“That may be the only silver lining here,” said Dr Pepper. “We’re going to learn some fundamentals about acute viral infections in people who haven’t been easy to study this way before.”
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