Molecular, Cellular, & Developmental Biology
Dr. Rui Yi
Herpes Simplex Virus type 1 (HSV-1) infects nearly 60% of the U.S. population, and is a significant cause of viral encephalitis and neuroinflammatory diseases. HSV-1 actively replicates in stratified epithelia, and then migrates to sensory neurons where it establishes a life-long, latent infection. It was recently demonstrated that HSV-1 can suppress exogenous RNA silencing, and viral replication is enhanced in the absence of Ago2. I investigated this further in a physiologically relevant in vitro epidermal cell culture model to determine if suppression of RNAi pathway components had any effect on HSV-1 replication, and if HSV-1 modulated endogenous miRNA silencing and expression. I found that deletion of Ago2 enhanced HSV-1 viral titers two to six-fold, and that the virus is capable of suppressing expression of mature miRNAs as well as their silencing function. These findings contribute to the nascent body of literature examining antiviral RNAi functions in mammals, and further our understanding of the epidermal response to one of the most common viral infections in the U.S.
Flagg, Meaghan, "Investigation of HSV-1 Interaction with the miRNA Pathway During Lytic Invection in Keratinocytes" (2013). Undergraduate Honors Theses. 351.