SARS-CoV-2 antibody-dependent enhancement of infection depends on antibody binding to both ACE2 and Fc receptors - PubMed

5 hours ago

Antibody-dependent enhancement (ADE) of infection is observed in viruses like dengue, Ebola, RSV, and HIV.
ADE occurs when virus-antibody complexes bind to Fc receptors (FcRs) and virus-specific receptors, enhancing infection under incomplete neutralization conditions.
The CoVIC study analyzed over 400 mAbs, comparing neutralization, Fc-mediated functions, receptor binding, and immune cell infection.
Macrophages showed higher susceptibility to SARS-CoV-2 and exhibited significant ADE with certain mAbs.
ADE was inhibited by FcR blockade and reduced by blocking ACE2 with antibodies or ceftazidime.
Neutralization potency did not correlate with ADE; both strongly and weakly neutralizing antibodies could induce enhancement.
ADE magnitude depended on an antibody's ability to block spike protein binding to ACE2.
ADE led to productive infection with release of infectious virus.
For the BA.1 (Omicron) variant, most mAbs showed reduced or lost ADE, while some had increased ADE compared to the USA-WA1/2020 strain.

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