Bacterial alteration of redox stressors impact environmental stability of Influenza A virus

Abstract

Influenza A virus (IAV) causes annual morbidity and mortality and remains a constant pandemic threat due to emergence of novel strains. Therefore, understanding the factors important in host-to-host transmission of IAV is a key control point for protecting individual and public health. Transmission is highly heterogeneous with viral factors and host inflammatory and immune factors being implicated. Also implicated is the upper respiratory microbiome. While typically thought to act indirectly on viral pathogenesis, in an immunomodulatory capacity to enhance or reduce susceptibility to viral infection, recent studies on the pathogenesis of IAV have identified direct interactions between the virus and upper respiratory pathobiont bacteria. We hypothesize that the bacterial cells and their metabolites co-shed into respiratory droplets with IAV particles, can alter the viability of the IAV particles in the environment, and therefore altering the capacity for host-to-host transmission. In this investigation we utilize a simplified model of fomite transmission in the absence of confounding host factors and demonstrate how oxidative stress from both the environment and the metabolic activity of S. pneumoniae contribute to the killing of IAV, while catalase or the metabolic activity of S. aureus can protect IAV from environmental or pneumococcally-produced reactive oxygen species.