Our Research
Decoding host factors to combat viral pathogenesis
Our research investigates host factors that shape viral pathogenesis, to advance therapeutics and guiding vaccine design
Enteroviruses are among the most common viruses that infect people around the world, costing the U.S. an estimated seven billion dollars each year. One member of this group, Coxsackievirus B3 (CVB3), can cause viral myocarditis, a serious heart infection that is fatal in about 5% of symptomatic cases. Despite their impact, there are currently no vaccines or treatments for Coxsackievirus infections. Our lab works to uncover how these viruses interact with the body and what factors shape the immune response, with the long-term goal of guiding new therapies and vaccine strategies to reduce disease and save lives.
Sex-bias in viral infections
Sex plays an important role in how people experience disease. In general, men are more vulnerable to infections, while women are more likely to develop autoimmune conditions. In our studies of CVB3, we found that male mice were more likely to develop severe disease than females, closely matching what is seen in humans. We also discovered that removing sex hormones reduced infection and disease, pointing to their influence in CVB3 pathogenesis. Our current work highlights testosterone as a key factor driving more severe disease in males and we are currently evaluating the differences between males and females in their immune response to CVB3.​
Virus-bacterial interactions
The bacteria living in our intestines can influence how viruses cause disease. In our work with Coxsackievirus B3 (CVB3), we found that certain gut bacteria and their cell wall components help the virus replicate, remain stable, and cause more severe illness. Surprisingly, the bacteria that support CVB3 differ from those that affect poliovirus, even though the two viruses are closely related. These findings show that each virus may rely on unique interactions with gut microbes to drive infection​​
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We thank our past and present funders
