High S1-specific IgA antibody levels discriminate severely ill SARS-CoV-2 patients. The virus acts as high avidity matrix for neutrophils to get activated via CD89 expressed on their membrane. Neutrophils start to produce LTB4 and undergo NETosis resulting in attraction and catching of more neutrophils resulting in amplification of the inflammatory response.
During infection local viral load is high ensuring a high-density epitope map for the IgA antibodies. Since IgAs have very strong effector functions this massive local neutrophilic activation causes collateral tissue damage resulting in severe lung disease.
Using the S1 IgA antibody level as companion diagnostic for treatment with antagonist anti-CD89 to prevent massive IgA driven pathology resulting in severe diseased patients.
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