Satish Pillai, PhD
Biography
My laboratory uses a systems biology approach to decipher the antiretroviral effects of IFN-α in vivo, by studying host gene expression, viral production and viral evolution in HIV-1-infected individuals undergoing IFN-α therapy. Recent data generated by our group strongly suggest that IFN-α 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 APOBEC3G, blocks HIV-1 infection by hyper-mutating the viral genome such that 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.
In addition to my principal research projects involving IFN-α and cell-intrinsic immunity, 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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- Satish Pillai, Benjamin Good, Douglas Richman, Jacques Corbeil. Sequence Note: A New Perspective on V3 Phenotype Prediction. AIDS Research and Human Retroviruses. 2003 Apr 1; 19(4):347-347.
- Coleman SH, Madrid R, Van Damme N, Mitchell RS, Bouchet J, Servant C, Pillai S, Benichou S, Guatelli JC. Modulation of cellular protein trafficking by human immunodeficiency virus type 1 Nef: role of the acidic residue in the ExxxLL motif. J Virol. 2006 Feb; 80(4):1837-49.
- Pillai SK, Kosakovsky Pond SL, Woelk CH, Richman DD, Smith DM. Codon volatility does not reflect selective pressure on the HIV-1 genome. Virology. 2005 Jun 05; 336(2):137-43.