Melanie Ott, MD, PhD
Senior Investigator, Gladstone Institute for Virology and Immunology
Melanie Ott Photo

Other Professional Titles

Professor, Medicine, University of California, San Francisco


(415) 734-4807


(415) 355-0855


Lauren Weiser
(415) 734-4809

On The Web

Areas of Investigation

Our laboratory focuses on virus-host cell interactions of two pathogens: the human immunodeficiency virus (HIV-1) and the hepatitis C virus (HCV). Specifically, we are interested in the molecular mechanisms of HIV transcription and latency, the central role of the HIV transactivator Tat and its control of transcription elongation, T cell activation and immune aging. In HCV research, we study the role of lipid droplets as an assembly platform for HCV virions and identify new host-viral protein interactions as potential therapeutic targets in infected liver cells. We recently developed a new focus on the role of reversible protein acetylation in autoimmunity with special emphasis on type I diabetes.

Lab Focus

Why is the triglyceride-synthesizing enzyme DGAT1, as opposed to its sister enzyme DGAT2, a target of HCV infection?
What is the comprehensive proteome of Tat modifications in infected cells?
What is the immune-regulatory function of SIRT1 in different T cell subsets and how is this immune-regulatory function inactivated during HIV-associated immune activation and autoimmunity?
What role does Tat play in the establishment and maintenance of HIV latency?


Discovered that the HCV core protein interacts with the triglyceride-synthesizing enzyme DGAT1 in HCV-infected liver cells and identified DGAT1 as a new critical cofactor for HCV infection.
Identified several posttranslational modifications in Tat, including acetylation and methylation that regulate interactions of Tat with TAR RNA and the transcription elongation factor P-TEFb.
Discovered that the transcriptional activity of P-TEFb is regulated by acetylation of four lysine residues in the coiled-coil region of the cyclin T1 subunit.
Found that Tat interacts and inhibits the NAD+ deacetylase SIRT1; this inhibition leads to enhanced acetylation of the p65 subunit of the NF-κB transcription factor contributing to generalized T cell activation in HIV infection.
Identified SIRT1 as a new regulator of regulatory T cell (Treg) function via deacetylation of the transcription factor FoxP3.


  • Association of American Physicians
  • American Association for the Advancement of Science
  • American Society for Microbiology
  • National Institutes of Health/National Institute of Allergy and Infectious Diseases, AIDS Molecular and Cellular Biology study section
  • Heinrich Pette Institute, Leibniz Institute for Experimental Virology (Scientific Advisory Board)
  • PLoS One (Editorial Board)

Professional titles

Professor, Medicine, University of California, San Francisco


  • University of Frankfurt/Main, Germany
  • Picower Graduate School Manhasset

Honors and Awards

2014 Avant-Garde Award, National Institutes of Health
2008 Sandler Opportunity Award, University of California, San Francisco
2008 UCSF Chancellor's Award for Public Service, University of California, San Francisco
2008 Thomas N. Burbridge Award, University of California, San Francisco
2006 Hellman Family Award, University of California, San Francisco
2000 Young Researcher Award, European Conference on Experimental AIDS Research, Madrid, Spain
1999 Young Research Award, European Conference on Experimental AID Research, Tampere, Finland
1991 Honors, Magna Cum Laude, University of Frankfurt/Main, Germany
1984 Scholarship, German National Merit Foundation