Satish Pillai, PhD
|School||UCSF School of Medicine|
|Address||270 Masonic Ave|
San Francisco CA 94118
Despite nearly three decades of focused research since the discovery of HIV-1, to date there is no cure or effective prophylactic vaccine for HIV-1 infection. Although the advent of Highly Active Antiretroviral Therapy (HAART) has dramatically decreased the morbidity and mortality associated with HIV-1 infection, there is a pronounced demand for alternative clinical management strategies due to frequent evolution of antiretroviral resistance, toxicity, and access constraints in resource-limited settings. My research is focused on identifying and characterizing novel host factors that act against HIV-1, by investigating the molecular determinants underlying the anti-HIV-1 activity of the antiviral cytokine interferon-alpha (IFN-a) in vivo. These host factors may serve as the foundations of future prophylactic, therapeutic and eradication strategies for HIV-1 infection.
Induction of IFN-a expression is a critical first step in the defense against a range of viral infections. The antiretroviral activity of the IFN-a cytokine was demonstrated in vitro almost immediately after the discovery of HIV-1, and includes inhibition of HIV-1 reverse transcription, viral assembly and virion release. Several clinical studies including our own report that IFN-a treatment acts against HIV-1 in vivo, and potently suppresses HIV-1 viremia in chronically-infected individuals. The precise molecular mechanisms underlying this suppressive activity in vivo, however, remain to be elucidated.
My laboratory uses a systems biology approach to decipher the antiretroviral effects of IFN-a in vivo, by studying host gene expression, viral production and viral evolution in HIV-1-infected individuals undergoing IFN-a therapy. Recent data generated by our group strongly suggest that IFN-a suppresses HIV-1 replication in chronically infected individuals by inducing intrinsic cellular inhibitors of retroviral replication known as host restriction factors. One of these factors, the cytidine deaminase APOBEC3, blocks HIV-1 infection by hypermutating the viral genome so it no longer encodes functional proteins that are necessary for viral replication. Another factor, the type 2 integral membrane protein BST-2/tetherin, blocks HIV-1 infection by restricting the release of fully formed progeny virions from infected cells. Our data warrant investigation into therapeutic strategies that specifically enhance the expression of these intrinsic immune factors in HIV-1-infected individuals. For a concise explanation of my latest research and its implications, please visit this new UCSF press release:
In addition to the my principal research projects involving IFN-a and host restriction factors, I participate as a bioinformaticist and phylogeneticist in a number of HIV/AIDS collaborations with researchers at the San Francisco VA Medical Center (SFVAMC), San Francisco General Hospital (SFGH) and the Gladstone Institute of Virology and Immunology (GIVI).
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