Antibody-dependent enhancement of SARS coronavirus infection and its role in the pathogenesis of SARS

Abstract

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.