Rachel Lent

Kaposi’s sarcoma-associated herpesvirus (KSHV) is a DNA virus that causes tumors in immunocompromised patients and is one the leading causes of cancer death in sub-Saharan Africa. The KSHV life cycle involves switching between a dormant (latent) and a replicative (lytic) cycle. The lytic cycle is essential for dissemination and tumor formation in a host, as well as for transmission to new hosts. Thus, it is important to understand factors that promote or limit lytic replication, as they are important for viral pathogenesis. Host innate immune responses, particularly type I interferon responses, are the first line of defense against viral infections and can limit KSHV replication. Interestingly, KSHV does not induce a strong type I interferon response upon lytic reactivation and thus evades its antiviral effects. Our lab has revealed that KSHV exploits cellular proteases called caspases to block antiviral interferon responses during lytic reactivation and promote viral replication. The goal of my research is to understand how KSHV lytic reactivation induces activation of cellular caspases to inhibit interferon induction. Studying these pro-viral processes can inform the development of therapies to prevent or treat KSHV-induced tumor formation and to control interferon responses in other settings.

Advisor: Marta Gaglia, PhD