MADRID, 14 Sep. (EUROPA PRESS) –
Hospitalized patients with COVID-19 are much more likely to harbor autoantibodies – antibodies directed at their own tissues or against substances their immune cells secrete into their blood – than people without COVID-19, according to a new study by researchers at the School of Stanford University Medicine (USA).
Autoantibodies can be precursors to an autoimmune disease. “If you get sick enough from COVID-19 to end up in the hospital, you may not be out of the woods even after you recover,” said PJ Utz, professor of immunology and rheumatology at Stanford Medicine and one of the authors. of the study.
Utz shares lead authorship of the study, which publishes ‘Nature Communications’, with Chrysanthi Skevaki, instructor of virology and laboratory medicine at Philipps University of Marburg in Germany, and Eline Luning Prak, professor of pathology and laboratory medicine at the University. from Pennsylvania.
Other lead authors of the study are Sarah Chang, a former Utz lab technician; Allen Feng, a recent Stanford graduate, now a technician in Utz’s lab; and senior research researcher Wenshao Meng, PhD, and postdoctoral scholar Sokratis Apostolidis, MD, both at the University of Pennsylvania.
The scientists looked for autoantibodies in blood samples drawn during March and April 2020 from 147 COVID-19 patients at the three university-affiliated hospitals and from a cohort of 48 patients at Kaiser Permanente in California. Blood samples drawn from other donors prior to the COVID-19 pandemic were used as controls.
The researchers identified and measured the levels of antibodies directed at the virus; autoantibodies; and antibodies directed against cytokines, proteins that immune cells secrete to communicate with each other and coordinate their overall strategy.
More than 60% of all hospitalized COVID-19 patients, compared to approximately 15% of healthy controls, carried anti-cytokine antibodies. This could be the result of an overload of the immune system caused by a persistent and virulent infection.
“In the fog of war, the abundance of cytokines can bypass the erroneous production of antibodies that attack them,” explains Utz. If any of these antibodies blocks the ability of a cytokine to bind to its appropriate receptor, the target immune cell may not be activated. That, in turn, could give the virus more time to replicate and lead to a much worse outcome.
TRACKING AUTOANTIBODIES
For about 50 patients, blood samples drawn on different days were available, including the day they were first admitted. This allowed the researchers to trace the development of the autoantibodies. “Within a week after checking into the hospital, about 20% of these patients had developed new antibodies against their own tissues that were not there on the day they were admitted,” explained Utz.
In many cases, he adds, “these autoantibody levels were similar to what would be seen in a diagnosed autoimmune disease.” In some cases, the presence of these newly detected autoantibodies may reflect an immune response-driven surge of antibodies that had been flying under the radar at low levels. It could be that the inflammatory shock in the systems of patients with severe COVID-19 caused an increase in the levels of previously undetectable, and perhaps harmless, autoantibodies that these individuals may have been carrying prior to infection.
In other cases, the generation of autoantibodies could result from exposure to viral materials that resemble our own proteins. “It is possible that, in the course of a poorly controlled SARS-CoV-2 infection, in which the virus lingers too long while an intensifying immune response continues to break the viral particles into pieces, the immune system sees fragments of the virus. viruses that I had not seen before, “says the researcher.
The finding strengthens the case for vaccination. COVID-19 vaccines contain just one protein, the so-called SARS-CoV-2 spike protein, or the genetic instructions for making it. With vaccination, the immune system is never exposed to the many new viral proteins generated during infection and is potentially not confused by them either.
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