Influenza virus is a respiratory pathogen of global importance with high economic and health-care burdens. This virus infects 10-20% of the population every year, causing an estimated one billion cases of disease, ~400,000 deaths, and an annual economic burden of billions of dollars.
Vaccines for influenza virus are available, however they fail to induce cross-reactive immunity and must be updated and re-administered every year to cover new variants. They are also insufficient to protect against emergent strains from zoonotic sources (e.g. avian influenza H5N1 and H7N9). As an alternative strategy to vaccines, health-care policies also aim to reduce the impacts of influenza by preventing virus transmission. However, an incomplete understanding of the complexity of transmission continues to hamper progress towards this goal. Upon exit from a host, influenza virus encounters an array of hostile environmental conditions (including a sharp humidity change and particle desiccation, high salinity, a pH decrease, and external factors of solar ultraviolet radiation and ozone).
Despite these stressors, infectious viruses are readily detected in exhaled aerosols from human patients. This indicates mechanisms of protection are at play. Respiratory matrices (e.g. mucin) are hypothesized to stabilize influenza virus against environmental inactivation outside the host, but the exact nature of this stabilization is only postulated. Furthermore, commensals of the respiratory niche pose another potential ‘stabilizer’ that have not comprehensively been examined. Binding interactions between enteric viruses and resident gut bacteria have been reported in the past, and are known to increase viral stability for a number of enteric viruses. Despite substantial microbial diversity in the respiratory tract, there has been limited research into similar pathogen co-operations, particularly from the perspective of virus stability during airborne transmission.
This project, which is led by Dr. Shannon David, seeks to unravel mechanisms of virus inactivation and persistence in this setting, to improve our capacity to control respiratory virus outbreaks in our future.
Collaborators:
Ulrich Krieger and Thomas Peter (ETHZ)
Athanasios Nenes (EPFL
Silke Stertz (UZH)
Oscar Vadas (University of Geneva)
Walter Hugentobler, General Physician
Funding: Swiss National Science Foundation