The way that HIV can do so much with so few genes is that each gene product is multifunctional, in a sense, HIV is the quintessential viral multi-tasker. Our work in this arena has contributed to describing the multiple functions of the HIV Tat protein. This, so-called, “accessory” viral protein is essential to the virus life cycle but also can re-direct cellular processes in un-infected cells. Soluble Tat, secreted from infected cells, is taken up by uninfected bystander cells via a protein transduction domain and can activate cell-adhesion molecule expression, inflammatory responses, apoptosis and cell proliferation, many of these through the induction of oxidative stress.

We are specifically interesting in understanding how this viral protein regulates oxidative, inflammatory and proliferative cellular responses in pulmonary vascular cells and the contribution of these aberrant responses to pulmonary arterial hypertension, which has a 1000-fold greater prevalence among people living with HIV (PLWH). Current research projects focus on investigating how Tat affects pulmonary vascular cell physiology either directly by transactivating host gene expression or indirectly by modulating the activity of cellular transcription factors.

Current support for our research comes from:

National Heart, Lung, and Blood Institute logo