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Dramatic levels of immune system “friendly fire” can fuel severe Covid-19 disease and leave patients with “prolonged Covid” when medical problems persist for a significant time after the virus has been beaten, they have said. the scientists.
Researchers at Yale University found that Covid-19 patients had a large number of the wrong antibodies in their blood that attacked organs, tissues and the immune system itself, rather than fighting the invading virus.
Scientists compared immune responses in patients and uninfected people and discovered dozens of aberrant antibodies in the former that blocked antiviral defenses, killed helpful immune cells, and attacked the body on multiple fronts, from the brain, blood vessels, and liver. down to the connective tissue. and the gastrointestinal tract.
Other tests revealed that the more “autoantibodies” patients had in their blood, the worse their disease. Covid-19 patients had more antibodies that had been turned against them than did people with lupus, an autoimmune disease caused by similar stubborn antibodies.
“Covid-19 patients produce autoantibodies that actually interfere with immune responses against the virus,” said Aaron Ring, a Yale immunobiologist and lead author of the study. Numerous other autoantibodies attacked parts of the body that are known to be damaged in people with the disease.
“We certainly believe that these autoantibodies are harmful to Covid-19 patients,” Ring said, adding that the harmful effects may continue after the infection has subsided, leaving patients with longer-lasting medical problems. “Because antibodies can persist for a long time, it is conceivable that they could contribute to the development of prolonged Covid diseases,” he said.
Ring partnered with Akiko Iwasaki, a professor of immunobiology at Yale, to screen 194 patients and hospital workers with varying degrees of Covid infection for autoantibodies targeting nearly 3,000 human proteins. Antibodies inactivate viruses by attaching themselves to proteins on the surface of the virus, but autoantibodies are incorrectly shaped and mistakenly bind to proteins found in or released from human cells.
Writing in the study, which has yet to be peer-reviewed and published in a journal, the scientists describe how Covid patients had “dramatic increases in autoantibody reactivities” compared to 30 healthy hospital workers who did not have the virus. While certain autoantibodies in some patients were apparently present prior to Covid-19 infection, others appeared and increased as the disease progressed.
More than 5% of hospitalized patients had autoantibodies that weakened a key arm of the immune defense that is orchestrated by proteins called interferons. These patients could not control the amount of virus in their bodies and therefore developed a more serious illness.
In two particularly grim examples of friendly fire, other patients had autoantibodies targeting B cells, the cellular factories that make antibodies to fight the virus, while one patient had autoantibodies that appeared to kill many of their protective T cells.
Rather than being to blame for one type of autoantibody, scientists believe that Covid-19 worsens when many different antibodies arise in the same patient. Tests in mice with some of the autoantibodies confirmed that they made the animals more susceptible to infection and more likely to die from the disease.
“The sum total of these multiple responses may explain a significant part of the clinical variation in patients,” the authors write.
Scientists have long known that conditions like rheumatoid arthritis, lupus, and multiple sclerosis are driven by a malfunction of the immune system and attacking the body. But less is known about viral infections and their ability to induce autoimmune reactions. Work is now underway to investigate whether autoantibodies are to blame for long-term symptoms in diseases like Ebola and chikungunya, and also in cancer patients after immunotherapy.
Ring said that if Covid-19 autoantibodies persist in the body, they could play a role in prolonged Covid. “Post-Covid syndromes could be caused by long-lasting autoantibodies that persist long after the virus is cleared from the body,” he said. “If so, there are immunosuppressive treatments, such as those used for rheumatologic diseases, that could be effective.” Long Covid is believed to affect approximately 10% of young people ages 18 to 49, increasing to one in five among those over 70.
Danny Altmann, a professor of immunobiology at Imperial College London, who was not involved in the study, said that autoantibodies could well explain the variety of Covid symptoms and the longer-lasting ailments that some patients experience.
“I think this is very likely, especially by analogy with Ebola and chikungunya, where autoimmunity seems to be a big part of the answer. A large part of our lab’s direction of travel for the next few months is trying to link long-term Covid symptoms to autoimmune profiles, ”he said.
