Abstract
<abstract> <p>The SARS-CoV-2 virus causes the COVID-19 disease associated with over 6.2 million deaths globally. Multiple early indicators raised the potential risk of the SARS-CoV-2 virus infecting monocytes and macrophages via Fc-receptor antibody binding based on closely related beta coronaviruses. Antibody Fc-receptor infection of phagocytic monocytes and macrophages is one type of antibody dependent enhancement of disease. Increased COVID-19 severity correlated with early high antibody responses on initial infection for unvaccinated adults. Clinical evidence suggests that for moderate antibody titer levels, antibodies binding to SARS-CoV-2 may contribute to viral spread, cytokine dysregulation, and enhanced COVID-19 disease severity. Primary immune responses appear to have too low of antibody titer to significantly contribute to Fc-receptor uptake by monocytes and macrophages for COVID-19 patients. Very high antibody titers created by SARS-CoV-2 vaccines also appear to inhibit Fc-receptor uptake and infection of monocytes and macrophages; this inhibition appears to decrease as antibody titer levels decrease. Cross reactive antibodies to other coronaviruses or moderate levels of SARS-CoV-2 antibodies may be contributing to antibody dependent enhancement of disease in critical COVID-19 patients.</p> </abstract>
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