Anti-respiratory syncytial virus (RSV) G monoclonal antibodies reduce lung inflammation and viral lung titers when delivered therapeutically in a BALB/c mouse model

RSV continues to be a high priority for vaccine and antiviral drug development. Unfortunately, no safe and effective RSV vaccine is available and treatment options are limited. Over the past decade, several studies have focused on the role of RSV G protein on viral entry, viral neutralization, and RSV-mediated pathology. Anti-G murine monoclonal antibody (mAb) 131-2G treatment has been previously shown to reduce weight loss, bronchoalveolar lavage (BAL) cell number, airway reactivity, and Th2-type cytokine production in RSV-infected mice more rapidly than a commercial humanized monoclonal antibody (mAb) against RSV F protein (Palivizumab). In this study, we have tested two human anti-RSV G mAbs, 2B11 and 3D3, by both prophylactic and therapeutic treatment for RSV in the BALB/c mouse model. Both anti-G mAbs reduced viral load, leukocyte infiltration and IFN-γ and IL-4 expression in cell-free BAL supernatants emphasizing the potential of anti-G mAbs as anti-inflammatory and antiviral strategies. •2B11 is a novel monoclonal antibody isolated from human PBMCs that binds RSV G.•In the BALB/c RSV challenge model, 2B11 reduces viral lung titers and inflammation when delivered prophylactically.•In the same model, 2B11 reduces viral lung titers when delivered three days post viral inoculation.•Anti-G mAbs reduced NK, B, and T cells in bronchoalveolar lavages when delivered three days post viral inoculation.•Anti-RSV G mAbs may enhance anti-F mAbs by providing additional anti-inflammatory characteristics.