Grant: Doctoral Research Award: Canada Graduate Scholarships

Respiratory Syncytial Virus (RSV) infection frequently leads to hospitalization and even death for infants and seniors. When these at-risk groups are weakened by RSV infection, they become susceptible to secondary bacterial infections. These respiratory co-infections are often caused by the bacteria Streptococcus pneumoniae, despite the availability of a pneumococcal vaccine. Co-infections are often more severe than one infection alone. There are no effective treatments for RSV, so there is a need to better understand RSV interactions with its host and other pathogens to develop new antiviral treatments. The human body has sensors that detect viruses and bacteria to initiate an immune response. However, our group has found that RSV takes advantage of the activation of a group of sensors called Toll-like Receptors (TLRs) to increase its replication. I am investigating whether TLR sensors that can be activated by both RSV and Streptococcus pneumoniae are responsible for the severe symptoms and outcomes observed during co-infection. My project will determine the precise components of TLR sensors that RSV exploits to amplify the severity of its infections and co¬infections. The molecules that I identify could serve as new drug targets so we can stop RSV from co-opting our immune response to reduce the burden of RSV and pneumococcal co¬infections.