Hong Kong Med J 2016;22(Suppl 4):S25-31
Antibody-dependent enhancement of SARS coronavirus infection and its role in the pathogenesis of SARS
MS Yip, HL Leung, PH Li, CY Cheung, I Dutry, D Li, M Daëron, R Bruzzone, JSM Peiris, M Jaume
HKU-Pasteur Research Pole, The University of Hong Kong
School of Public Health, The University of Hong Kong
1. Anti-SARS-CoV spike antibodies promote infection of primary human immune cells by SARS-CoV.
2. The antibody-dependent enhancement (ADE) infection pathway grants SARS-CoV an opportunity to infect primary human macrophages, but it does not sustain productive viral replication in the infected cells.
3. ADE of SARS-CoV infection does not alter pro-inflammatory gene expression profile of primary human macrophages.
4. Infectivity of SARS-CoV does not rely solely on the potency of target cells to bind — via Fcγ receptor II (CD32) — infectious immune complexes, but depends on the properties of the intracellular domain of the FcγRII.
5. Occurrence of ADE of SARS-CoV infection into human primary macrophages, without alteration to their pro-inflammatory properties, advocates cautious development of SARS-CoV vaccine in humans, and provides new ways of investigation to understand the pathogenesis of SARS.