Researchers, including one of Indian-origin, have identified that the COVID-19 virus may prompt the body to make weapons to attack its own tissues.

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According to the researchers, including Saborni Chakraborty from Stanford University in the US, the finding could unlock a number of COVID-19's clinical mysteries. "It suggests that the virus might be directly causing autoimmunity, which would be fascinating," said lead author Paul Utz from the varsity. For the study, preprinted in medRxiv, the research team included data from more than 300 patients from four hospitals and used blood tests to study their immune responses as their infections progressed.

They looked for autoantibodies -- weapons of the immune system that go rogue and launch an attack against the body's own tissues. They compared these autoantibodies to those found in people who were not infected with the virus that causes COVID-19. As previous studies have found, autoantibodies were more common after COVID-19 -- 50 percent of people hospitalised for their infections had autoantibodies, compared to less than 15 percent of those who were healthy and uninfected, WebMD reported.

Some people with autoantibodies had little change in them as their infections progressed. That suggests the autoantibodies were there to begin with, possibly allowing the infection to burn out of control in the body. But in others, about 20 percent of people who had them, the autoantibodies became more common as the infection progressed, suggesting they were directly related to the viral infection, instead of being a pre-existing condition.

Some of these were antibodies that attack key components of the immune system's weapons against the virus, like interferon, suggests the study, to be peer reviewed. Interferons are proteins that help infected cells call for reinforcements and can also interfere with a virus's ability to copy itself. "Our studies have begun to quantify the impact of SARS-CoV-2 on autoimmunity, identifying which antigens and specific autoimmune diseases to surveil in patients who have been infected, and contributing to our mechanistic understanding of COVID-19 pathogenesis," the researchers said.