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A hallmark of many autoimmune diseases, autoantibodies wreak havoc by recognizing and interfering with the body’s own proteins, DNA, and other molecules, known altogether as self-antigens.
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Evidence of a link between autoantibodies and long COVID symptoms is also building. Among the most incriminating are autoantibodies that bind to cell surface proteins called G-protein coupled receptors (GPCRs) and may block the messages these proteins convey to cells to control immune and other functions. Various GPCR antibodies are thought to contribute to ADs including ME/CFS, rheumatoid arthritis, and Sjogren’s syndrome. Last spring, a small study of individuals experiencing long COVID symptoms—particularly neurological (fatigue, etc) and cardiovascular (elevated heart rate, etc)—found that all had GPCR autoantibodies [9].
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If it can be demonstrated that certain autoantibodies are associated with specific symptoms of long COVID, “that would help strengthen the case” that there is an underlying autoimmune cause, Dr. Luning Prak says. In the context of acute COVID-19, there is evidence of autoantibodies targeting a range of self-antigens in the lungs, central nervous system, and other organs that have been implicated in long COVID disease.
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Last year, doctors gave a 59-year- old man an experimental drug for his glaucoma that blocks GPCR autoantibodies [17]. The patient also suffered from long COVID and had autoantibodies against GPCRs. In addition to improvements in his glaucoma, the man recovered from fatigue, brain fog, and loss of taste for at least 4 weeks.