Melanie Ott, MD, PhD

Senior Investigator

Phone: (415) 734-4807
Fax: (415) 355-0855
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Professor, Medicine, University of California, San Francisco

Administrative Assistant

Veronica Fonseca
(415) 734-4809

More about Dr. Ott

Dr. Ott’s research focuses on two pathogens—the human immunodeficiency virus (HIV-1) and the hepatitis C virus (HCV)—and how these viruses interact with the cells of a host. More specifically, she studies the molecular mechanisms by which HIV infects and replicates in CD4 T cells, wreaking havoc on a segment of the body’s immune system. In HCV research, Dr. Ott is examining ways in which HCV viral particles assemble within liver cells—in an attempt to understand the interactions between viral proteins, fat metabolism and mitochondria in these infected cells.

Dr. Ott joined GIVI in 2002 as a Visiting Investigator, later becoming a Staff Research Investigator and then a Senior Investigator.  

In both 1999 and 2000, Dr. Ott was honored with the Young Researcher Award at the European Conference on Experimental AIDS Research. In 2006, she won the Hellman Award, established by F. Warren Hellman at UCSF to support the research of promising assistant professors with the capacity for great distinction in their research. She is also a recipient of the Chancellor’s Award for Public Service with UCSF for her work as founder and co-chair of the student-outreach committee at Gladstone. The committee promotes science education in local schools and specifically targets underserved youth.

Dr. Ott is a member of many scientific and professional societies, including the Association of American Physicians. She also serves as a permanent member of the AIDS Molecular Cellular Biology study section at the National Institutes of Health and is a member of scientific advisory boards of several scientific institutions, including the Pette Institute of Virology and the Helmholtz organization in Germany. Prior to joining Gladstone, Dr. Ott started her own research group at the German Cancer Research Center in Heidelberg, Germany.

A native of Germany, Dr. Ott earned an MD from the University of Frankfurt/Main, Germany, and a PhD in molecular medicine from the Picower Graduate School in Manhasset, New York.

More scientific details, please

Other Professional Titles

Professor, Medicine, University of California, San Francisco

Administrative Assistant

Veronica Fonseca
(415) 734-4809

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.

Current 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?

Joined Gladstone


Why Gladstone?

Gladstone provides the rich and vibrant research environment critical for the success of our highly collaborative research; we enjoy close and interdisciplinary interactions with our colleagues at Gladstone, UCSF and other Bay Area universities and benefit from the climate of scientific excellence and collegiality here at Gladstone.

Key Achievements

  • 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.


University of Frankfurt/Main, Germany (MD), with Honors, Magna Cum Laude (1991)
Picower Graduate School Manhasset (PhD) (1997)


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, Member, Scientific Advisory Board
Editorial Board, PLoS One


  • Scholarship, German National Merit Foundation (1984)
  • Young Research Award, European Conference on Experimental AID Research, Tampere, Finland (1999)
  • Young Researcher Award, European Conference on Experimental AIDS Research, Madrid, Spain (2000)
  • Hellman Family Award, University of California, San Francisco (2006)
  • 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 (2008)
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Featured Publications

Melanie Ott, MD, PhDHarris C, Herker E, Farese RV Jr, Ott M. Hepatitis C virus core protein decreases lipid droplet turnover: a mechanism for core-induced steatosis. J Biol Chem. 2011 Dec 9;286(49):42615-25. Epub 2011 Oct 7. View in: PubMed
Melanie Ott, MD, PhDHerker E, Harris C, Hernandez C, Carpentier A, Kaehlcke K, Rosenberg AR, Farese RV Jr, Ott M. Efficient hepatitis C virus particle formation requires diacylglycerol acyltransferase-1. Nat Med. 2010 Nov;16(11):1295-8. Epub 2010 Oct 10. View in: PubMed