No Evidence for Human Monocyte-Derived Macrophage Infection and Antibody-Mediated Enhancement of SARS-CoV-2 Infection

• Published in: Frontiers in cellular and infection microbiology Vol. 11; p. 644574
• Main Authors: García-Nicolás, Obdulio, V'kovski, Philip, Zettl, Ferdinand, Zimmer, Gert, Thiel, Volker, Summerfield, Artur
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 12.04.2021
• Subjects: ADE; Cellular and Infection Microbiology; COVID-19 convalescent sera; human coronaviruses; human monocyte-derived macrophages; SARS-CoV-2; human monocyte-derived macrophages; ADE; SARS-CoV-2; COVID-19 convalescent sera; human coronaviruses
• ISSN: 2235-2988; 2235-2988
• DOI: 10.3389/fcimb.2021.644574

Vaccines are essential to control the spread of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and to protect the vulnerable population. However, one safety concern of vaccination is the possible development of antibody-dependent enhancement (ADE) of SARS-CoV-2 infection. The potential infection of Fc receptor bearing cells such as macrophages, would support continued virus replication and inflammatory responses, and thereby potentially worsen the clinical outcome of COVID-19. Here we demonstrate that SARS-CoV-2 and SARS-CoV neither infect human monocyte-derived macrophages (hMDM) nor induce inflammatory cytokines in these cells, in sharp contrast to Middle East respiratory syndrome (MERS) coronavirus and the common cold human coronavirus 229E. Furthermore, serum from convalescent COVID-19 patients neither induced enhancement of SARS-CoV-2 infection nor innate immune response in hMDM. Although, hMDM expressed angiotensin-converting enzyme 2, no or very low levels of transmembrane protease serine 2 were found. These results support the view that ADE may not be involved in the immunopathological processes associated with COVID-19, however, more studies are necessary to understand the potential contribution of antibodies-virus complexes with other cells expressing FcR receptors.