The role of respiratory syncytial virus G protein in immune cell infection and pathogenesis.

Abstract

Severe respiratory syncytial virus (RSV) disease is a significant contributor to the global burden of disease in infants and children. The RSV attachment protein (G) has been shown to be critical in invading airway epithelial cells through its CX3C motif interacting with the host receptor CX3CR1. The ubiquitous expression of this receptor on immune cells may explain their susceptibility to RSV infection. The RSV G protein may enhance disease severity through reprogramming of normal cellular functionality leading to inhibition of antiviral responses. While existing preventives targeting the RSV fusion (F) protein are highly effective, there are no RSV therapeutics based on the G protein to limit RSV pathogenesis. Monoclonal antibodies targeting the RSV G protein administered as post-infection therapeutics in mice have been shown to improve the antiviral response, reduce viral load and limit disease severity. Further research is required to better understand how RSV infection of immune cells contributes to pathogenesis for the development of more targeted and efficacious therapeutics.