ABSTRACT The coronavirus disease 2019 (COVID-19) pandemic has raised concerns about the detrimental effects of antibodies. Antibody-dependent enhancement (ADE) of infection is one of the biggest concerns in terms of not only the antibody reaction to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) upon reinfection with the virus but also the reaction to COVID-19 vaccines. In this study, we evaluated ADE of infection by using COVID-19 convalescent-phase plasma and BHK cells expressing human Fcγ receptors (FcγRs). We found that FcγRIIA and FcγRIIIA mediated modest ADE of infection against SARS-CoV-2. Although ADE of infection was observed in monocyte-derived macrophages infected with SARS-CoV-2, including its variants, proinflammatory cytokine/chemokine expression was not upregulated in macrophages. SARS-CoV-2 infection thus produces antibodies that elicit ADE of infection, but these antibodies do not contribute to excess cytokine production by macrophages.
【저자키워드】 COVID-19, SARS-CoV-2, macrophages, Antibody-dependent enhancement, ADE, FcγRIIA, FcγRIIIA, 【초록키워드】 coronavirus disease, antibodies, coronavirus, pandemic, antibody, SARS-COV-2 infection, Infection, virus, variants, proinflammatory, Reinfection, COVID-19 vaccines, plasma, receptor, cytokine production, acute respiratory syndrome, Cell, evaluated, raised, contribute, elicit, upregulated, expressing, detrimental effect, cytokine/chemokine expression, FcγRs, infected with SARS-CoV-2, monocyte-derived macrophage, 【제목키워드】 Production, IgG, enhancement, Mediated,