Benjamin A. Krishna

The paper identifies CD8+ T cell epitopes in HAdV-F40 and F41 hexon and penton proteins, showing they elicit IFNγ responses in healthy donors and could inform vaccine design.

This study identifies UL78 as a viral factor that facilitates the switch from latency to reactivation in CMV-infected myeloid cells by modulating cellular signaling.

This study shows that inhibiting MAPK signaling suppresses CMV reactivation in CD34+ Kasumi-3 cells, suggesting a therapeutic target for preventing viral reactivation in immunocompromised patients.