We are studying how our response to the flu might leave us susceptible to bacterial superinfection.

The term “bacterial superinfection” can be a bit intimidating, but its clinical definition is actually pretty ordinary. It’s a bacterial infection that you get on top of an infection you already have (caused by bacteria, viruses or even fungi).

Tens of thousands in the U.S. die each year from influenza and most of those deaths are caused by a bacterial superinfection. However, one question remains as to why doesn’t every flu infection lead to a bacterial superinfection?

To answer this question we looked into how the flu virus can manipulate our immune response. Specifically, a group of proteins called cytokines, which are used in cell communication and drive the body’s immune response.

We found that some cytokines, known as interferons, can be manipulated by influenza viruses. This can make the host more or less vulnerable to superinfection. This depends upon the specific strain of influenza.

In this project we’re seeking to determine how and why some influenza viruses disrupt our cytokine signaling, thereby determining susceptibility to post-influenza bacterial superinfection.

Once we better understand how the body interacts with an influenza virus, we will be able to manipulate these triggers to reduce superinfection susceptibility and stimulate protective responses. Preventing superinfection will help to save lives.