Keeping the heart protected from Influenza A virus comes down to T cells
Influenza A virus (IAV) infection primarily affects the lungs, but is often also found in heart tissue, specifically in people with severe infections who go on to experience cardiac complications. A substantial number of patients hospitalized with influenza display signs of myocarditis, or inflammation of the heart tissue. Researchers in the Yount Laboratory in The Ohio State University College of Medicine aim to understand and combat cardiac influenza virus infections.
Previous work in the Yount Laboratory has shown that cardiac muscle cells are directly infected by IAV, therefore driving heart dysfunction and fibrosis. A grant from the American Heart Association (AHA), will now help researchers in that lab uncover the mechanisms involved in affecting how the virus arrives in the heart and how the body effectively clears the virus from the heart.
“Understanding the mechanisms of influenza A virus infection and clearance from the heart” will test the hypothesis that the movement of IAV from the lungs to the heart is facilitated by movement of infected immune cells by using an engineered influenza virus with specific attenuation for immune cells to broadly evaluate the involvement of immune cell infection in cardiac pathogenesis.
Led by Jack Roettger, an AHA Predoctoral Fellow and a PhD candidate in the Yount Lab, the research team will also delete specific cell populations that play a crucial role in the function of the immune system.
“This will enable us to decode specific cell types responsible for trafficking [the] virus to the heart and help us understand how the immune system successfully clears cardiac infection in most healthy individuals and why it doesn’t in cases of infection-related cardiac pathology,” Roettger says.
Roettger explains that their knowledge of CD4+ and CD8+ T cells playing a role in the effective control of other cardiotropic viruses, as well as IAV infection in the lungs, led them to conclude that cardiac IAV clearance comes down to T cells.
“We’ve confirmed the presence of virus-specific T cells in the heart during infection,” Roettger says. “Now we will dig deeper into the biological activity of these virus-specific cardiac T cell populations and the role of CD8+ cytotoxicity on virus clearance and cardiac damage/dysfunction during infection.”
Roettger stresses the importance of flu vaccination, by noting that cardiac events increase during flu season, particularly in the unvaccinated. The AHA also recommends yearly flu vaccination, an increasingly critical measure for those with a history of cardiovascular events, such as heart disease or stroke.
Uncovering the mechanisms underlying cardiac pathology caused by IAV has the potential to develop new preventive and therapeutic efforts and offer hope to the segment of the world’s population — nearly 10% — that becomes infected with IAV each year.
