Infection enhancement of influenza A NWS virus in primary murine macrophages by anti‐hemagglutinin monoclonal antibody

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Abstract
Antibody-dependent enhancement (ADE) of influenza A NWS virus infection was investigated in primary murine macrophages (Mø,) using antihemagglutinin(HA) monoclonal antibody (mAB). Contrary to previous reports of abortive influenza virus infection in primary Mø, this study demonstrated that the NWS virus replicated productively in both resident peritoneal Mø, and thioglycolate-elicited peritoneal Mø, providing cleavage of the HA was achieved by trypsin; 5 μMg/ml of trypsin was the optimum concentration for the induction of infectivity. Under multiplecycle growth conditions in the presence of mAB at various concentrations in trypsin-containing media, ADE was demonstrated in both Mø, in the presence of subneutralizing concentrations of mAB. Flow cytometric analysis showed that the mechanism of virus entry into Mø, could be through HA to specific virus receptors, or HA plus antibody to Fc receptors. These results indicate that ADE of the NWS virus infection actually occurs on Fc receptor-bearing primary murine Mø, depending on the concentration of antibody in the presence of the appropriate protease for cleavage of viral HA.