We are interested in how viruses interact with the host cell; through these interactions we hope to gain new insight into cellular processes and the viral life cycle. Currently, we focus on two pathogens—the human immunodeficiency virus (HIV-1) and the hepatitis C virus (HCV)—and three cellular processes—lipid droplets, transcriptional elongation, and chronic immune activation. Our research is relevant for efforts to eradicate HIV from patients, to alleviate fatty liver disease in chronic HCV infection, and suppress autoimmunity in patients with Type 1 Diabetes.
Lipid droplets (LDs) are highly dynamic cellular organelles involved in energy homeostasis and membrane trafficking. Several RNA viruses, including HCV and Dengue Virus, use host LDs at different steps of their life cycle. Although many mechanistic details of the LD:virus interaction are unknown, a picture emerges in which the unique cellular architecture and energy stored in LDs are important in the replication of a diverse range of viruses.
Latently infected memory T cells represent a major barrier to eradicating HIV from infected individuals, and efforts are underway to reverse HIV latency in an attempt to cure HIV-infected individuals. By understanding molecular mechanisms regulating HIV transcription and identifying new factors involved in its regulation, we contribute to worldwide efforts to eradicate HIV and gain new insights into the molecular regulation of transcription elongation in the cell.
Persistent pathogens like HIV cause a state of chronic immune activation linked to premature immune aging and shortened life/health span. Our goal is to develop novel therapies designed to slow immune aging by gaining insight into shared pathways linking HIV infection with chronic immune activation. Special emphasis lies on epigenetics, T cell metabolism, and potential parallels with other chronic immune activation diseases such as autoimmunity.