Our lab’s interests lie in dissecting how viruses interface with the pathways that govern messenger RNA turnover.  The ability to regulate RNA stability has the potential to impact gene expression on a global scale, but is also critical for fine-tuning cellular responses to specific stimuli as well as eliminating flawed and potentially deleterious transcripts.  We seek to pinpoint viral targets within these pathways so as to better understand mechanisms by which viruses regulate their own messages and/or eliminate potentially competitive or antiviral cellular transcripts.  We anticipate that these studies will also enhance our understanding of how such important pathways are normally regulated in human cells.

Our models are γ-herpesviruses such as Kaposi’s sarcoma-associated herpesvirus (KSHV), as these agents promote global cellular mRNA destruction during their lytic replication cycle.  A critical viral effector of this phenotype is called SOX (encoded by ORF37 in KSHV and MHV68).  We hypothesize that SOX deregulates one or more cellular RNA degradation pathways to achieve host shutoff.