Viruses reshape the intracellular environment during infection, both to hijack processes necessary for viral amplification and to subvert antiviral defenses. Because of size constraints and competition with their hosts for resources, they have developed ingenious ways to benefit from the host gene expression machinery. As such, viruses are excellent tool to understand cell biology.

Herpesviruses are a particularly good example of such successful balance as herpesvirus infections are life-long and cannot be cleared by the host. We focus on the Gamma-herpesviruses and in particular, KSHV (Kaposi Sarcoma Associated Herpesvirus). KSHV is a major focus of research, as its namesake disease Kaposi’s Sarcoma is one of the most common and aggressive cancers in untreated AIDS patients.

The success of KSHV replication is heavily reliant on its ability to exert strong control over the gene expression machinery of the infected cell.
During the lytic cycle, KSHV drives a dramatic remodeling of the host cell gene expression environment. The signature event underlying many of the gene expression changes is the widespread depletion of cytoplasmic mRNA. RNA decay is triggered by the KSHV encoded endoribonuclease SOX and it is estimated that up to 70% of total mRNA are affected by this process.

We focus on the 30% of transcripts that are escaping this viral-induced widespread RNA decay and we are in the process of understanding how and why these transcripts escape degradation. Our research is therefore heavily reliant on understanding the RNA biology of select transcripts during infection (turnover, localization, RNA-protein complex) while addressing fundamental viral-host interplay questions.

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