Research

Infection with Human Cytomegalovirus (HCMV), a ubiquitous pathogen in the general population, causes little to no symptoms in healthy individuals. However, the virus can cause severe morbidity and mortality within the immunosupressed and immunocompromised populations. HCMV is a very large (240kB) herpesvirus that encodes up to 200 ORFs which are expressed in a very regulated transcriptional cascade. HCMV, as all herpesviruses, maintains the ability to enter into latency where viral transcription is silenced and the virus remains in a quiescent state while retaining the ability to reactivate as environmental conditions within a host change. Understanding the progression of pathogenesis induced by HCMV is the focus of the laboratory, specifically investigating different factors that regulate the lifecycle of the virus, and how these factors may regulate the maintenance of latency.

My laboratory has identified small RNA transcripts (microRNAs), encoded by both the human genome and the viral genome, that target proteins essential for efficient viral replication. Additionally, we have identified several cellular proteins which are targets for viral encoded microRNAs including factors involved in inducing apoptosis. Current research involves studying the importance of these microRNA induced changes within the cellular environment in relation to the virus lifecycle.