A recent study published in the Journal of Virology by a team from the Department of Molecular Biology and Biochemistry that includes Assistant Professor Roberto Tinoco, graduate student Julia DeRogatis and co-authors from the Tinoco lab, and Assistant Professor Dequina Nicholas has revealed a new discovery about how T cells respond to viral infections. The study focused on CD8+ T cells, which help our bodies recognize and kill virus-infected cells.
During chronic viral infection, CD8+ T cells become exhausted over time, losing much of their ability to fight the ongoing infection. The researchers uncovered that a protein called CD38 is present at high levels on exhausted CD8+ T cells during chronic viral infection and went on to investigate the function it played on these cells.
The researchers found that CD38 has a dual role in virus-specific CD8+ T cells. On the one hand, CD38 limits T cell proliferation as well as the production of cytotoxic killer proteins. On the other hand, CD38 helps CD8+ T cells survive and provides them with the metabolic energy they need to keep fighting the virus. Overall, the researchers showed that in chronic viral infection, CD38 limits virus specific CD8+ T cell functions, but ultimately supports their metabolism and survival over the course of infection.
These findings could be important for developing new immunotherapies to help fight viral infections in humans. By understanding how CD38 affects CD8+ T cells, researchers might be able to develop treatments that improve survival and function of virus-responding T cells. This study helps us better understand how our bodies fight viral infections and provides a potential new target for future treatments.
Read the full paper here.