Ott has worked to understand HIV transcription and viral latency within host cells as targets to eradicate the spread of the virus. HIV inserts its genome into its host cell's DNA; in this form, the virus is known as a provirus. While antiretrovial drugs are able to prevent the spread of actively transcribed and replicating HIV, they cannot target HIV provirus that is laying dormant in the host genome. Eliminating latent provirus is therefore essential for eradicating the virus. Ott and her team have worked on developing a "shock and kill" strategy to reactivate and flush out latent HIV provirus so that the immune system and antiretroviral drug therapies can kill off dormant viruses. Her laboratory has been exploring repurposing cancer drug therapies that target epigenetic machinery to reactivate latent HIV provirus. They have studied both the effect of inhibiting the function of deacetylases to loosen the host's heterochromatin structures to restart HIV transcription and of activating the viral transcription protein Tat. In a 2017 study, they targeted the human enzyme SMPD2, which allows HIV to remain latent. They were able to reactivate latent provirus in about one-quarter of human cells donated by HIV patients.
COVID-19 research
Ott is a member of UCSF's Quantitative Biosciences Institute's COVID consortium. In the wake of the COVID-19 pandemic, Ott and her team of collaborators worked to reequip and recertify an unused biosafety level 3research laboratory at University of California, San Francisco in order to study SARS-CoV-2, the virus responsible for coronavirus disease 2019. A BSL-3 laboratory allows researchers to study infectious agents, such as the novel coronavirus, which can cause serious diseases in humans. Her team also received training in how to work with the virus without risking infection, though Ott has commented to the press that the limited stock of personal protective equipment is a cause for concern as they proceed with their research. Ott and her team began working to understand how coronaviruses reproduce in a host in order to understand how to disrupt the virus's life cycle using drugs. They began infecting lung organoids with the virus to both understand its pathogenesis, as well as identify potential drugs to stop its spread. She is also collaborating with Jennifer Doudna at University of California, Berkeley to develop a rapid CRISPR-based diagnostic test for the virus that would show results within 30 minutes.
Selected publications
"Metabolic reprogramming of human CD8+ memory T cells through loss of SIRT1." Journal of Experimental Medicine. 2018 Jan 2;215:51-62. doi:
"The Short Isoform of BRD4 Promotes HIV-1 Latency by Engaging Repressive SWI/SNF Chromatin-Remodeling Complexes." Molecular Cell 2017 Sep 21;67:1001-1012.e6. doi:
"A combined proteomics/genomics approach links hepatitis C virus infection with nonsense-mediated mRNA decay." Molecular Cell 2015 Jan 22;57:329-340. doi:
"Acetylation of RNA Polymerase II Regulates Growth-Factor-Induced Gene Transcription in Mammalian Cells." Molecular Cell 2013 Nov 7;52:314-24. doi:
"Efficient hepatits C virus particle formation requires diacylglycerol acyltransferase-1." Nature Medicine 2010 Nov;16:1295-8. doi:
Awards and honors
Young Researcher Award, European Conference on Experimental AIDS Research, 2000
F. Warren Hellman Award, University of California, San Francisco, 2006
Chancellor's Award for Public Service, University of California, San Francisco, 2008