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

Infection with SARS-CoV involves not only the respiratory tract but also the gastrointestinal tract and other organ systems. Several reports have highlighted the direct infection of haematopoietic cells by SARS-CoV. It is unclear how the virus gets into immune cells that do not express the SARS-CoV receptor angiotensin I converting enzyme 2 (ACE2). Immune-mediated infections and, in particular, antibody-dependent enhancement (ADE) is known to be exploited by a variety of viruses, such as dengue virus, HIV, and animal coronavirus, as an alternative way to infect host cells.1 In addition to an interaction between viral protein and host receptors, these viruses can enter cells through the binding of virus/ antibody immune-complexes to Fc receptors (FcR), complement receptors, or alternatively by inducing conformational change in envelope glycoproteins that are required for virus-cell membrane fusion.1 We have demonstrated that anti-spike antibodies potentiate infection of both monocytic and lymphoid human immune cell lines with SARS-CoV Spike-pseudotyped lentiviral particles (recombinant viruses encoding a reporter gene and bearing SARS-CoV Spike proteins at the virion surface; SARS-CoVpp) and also with replicationcompetent SARS-coronavirus.2 Because antibodyHong Kong Med J 2016;22(Suppl 4):S25-31 RFCID project number: 09080872