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Concentrations of autoantibodies correlate with disease severity.
Why do some people get so much sicker than others with acute COVID-19? And what causes the neurological symptoms — anosmia, fatigue, encephalopathy — seen in some patients? A team from Yale employed a new technology for finding autoantibodies to 2770 extracellular and secreted proteins. They tested 172 patients with severe COVID-19 at one Connecticut hospital, 22 healthcare workers who had mildly symptomatic or asymptomatic COVID-19, and 30 healthcare workers who were negative for COVID-19.
Compared with uninfected patients, patients with COVID-19 had many more autoantibodies, including antibodies directed at immune-system molecules involved in defense against viral infection. This was particularly true in patients with more severe illness. This study confirms previous reports that autoantibodies against type I interferons are associated with more severe disease (NEJM JW Gen Med Jan 1 2021 and Science 2020; 370:4570). Autoantibodies also were directed against blood vessels and multiple organs, including the central nervous system. In particular, having autoantibodies that inhibit the receptor for orexin (a peptide that regulates arousal) correlated strongly with low Glasgow Coma Scale score.
The same investigators studied paired cerebrospinal fluid (CSF) and blood from a small group of COVID-19 patients. They found many autoantibodies against SARS-CoV-2 that also react with neural targets, particularly autoantibodies in cerebrospinal fluid. One such antibody attacks a target that is involved in smell. These autoantibodies were abundant, even in patients without classical markers of neuroinflammation such as pleocytosis.
New technologies allow identification of many autoantibodies. Their abundance in people with COVID-19 suggests that they could affect both severity and symptoms of the disease.
Créditos: Comité científico Covid