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Satish PillaiSatish K. Pillai, PhD

Current Positions:

  • Associate Investigator, BSRI
  • Associate Adjunct Professor, UCSF Department of Laboratory Medicine
  • Associate Director, UCSF-GIVI Center for AIDS Research (CFAR)

Contact Information:
270 Masonic Ave.
San Francisco, CA 94118
Phone: (415) 513-4461
Fax: (415) 567-5899
Email: spillai@bloodsystems.org

 

 

Download a scientific summary [pdf file]

Download a curriculum vitae [pdf file]

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Link to UC Berkeley web profile (Understanding Evolution)
http://evolution.berkeley.edu/evolibrary/article/0_0_0/pillai_01

Link to UCSF press release: “Fighting Infections: Old Drug Reveals New Tricks”
http://www.ucsf.edu/news/2012/02/11598/fighting-infections-old-drug-reveals-new-tricks

Link to a video of an interview at the California Academy of Sciences
https://vimeo.com/34239567
 

Education:

  • B.S., Ecology & Evolutionary Biology, University of Arizona
  • Ph.D, Evolutionary Biology, University of California, San Diego

Training / Appointments:

  • Graduate Research Assistant, HIV Sequence Database, Los Alamos National Laboratory
  • Postdoctoral Fellow, UCSF Department of Medicine
  • Postdoctoral Teaching Fellow, UCSF Medical School
  • Assistant Adjunct Professor, UCSF Department of Medicine, Division of Infectious Diseases
  • Staff Investigator, San Francisco VA Medical Center
  • Visiting Scientist, Gladstone Institute of Virology and Immunology
  • Research Associate, Center for Comparative Genomics, California Academy of Sciences
  • UCSF AIDS Research Institute (ARI) Executive Committee Member
  • Chair, UCSF Resource Allocation Program (RAP) Basic HIV/AIDS, Infectious Diseases & Global Review Committee
     

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Research Interests:

  • Viral genetic determinants of HIV pathogenesis and persistence
  • Effects of interferon-mediated immunity on viral latency and evolution
  • Estimation of HIV incidence using novel biomarkers
     

Current Research:

  • To date, there is no cure or effective prophylactic vaccine for HIV-1 infection. Although the advent of antiretroviral therapy (ART) 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 lab is largely 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-α) in vivo. These host factors may serve as the foundations of future prophylactic, therapeutic and eradication strategies for HIV-1 infection.

    Induction of IFN-α expression is a critical first step in the defense against a range of viral infections. The antiretroviral activity of the IFN-α 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-α 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-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 hypermutating 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. For a concise explanation of our recent research and its implications, please visit this UCSF press release:

    http://www.ucsf.edu/news/2012/02/11598/fighting-infections-old-drug-reveals-new-tricks

    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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Publications:

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