Steven Yukl, MD | Biomedical Sciences Graduate Program

Professor in Residence

Department of Medicine - Infectious Disease

Primary Thematic Area

Secondary Thematic Area

Research Summary

My research aims to understand the barriers that prevent HIV cure, with a focus on determining the mechanism governing latent HIV infection and evaluating new therapies aimed to disrupt viral latency.

[email protected]

+1 415 221-4810 ext. 3930

I am a physician-scientist at UCSF and the San Francisco VA. Since 2005, I have been conducting laboratory-based research aimed at understanding the barriers to curing HIV. My laboratory focuses on investigating the mechanisms that allow HIV to establish a latent infection (which is widely regarded as the main barrier to curing HIV) in the blood and tissues. After the start of the COVID-19 pandemic, we also became interested in the transcriptional regulation of SARS-CoV-2, another RNA virus. We are currently investigating how SARS-CoV-2 subgenomic transcription (which is analogous to RNA splicing) allows for variation in the expression of different coronavirus genes over time, and how these SARS-CoV-2 subgenomic RNAs interact with human cells to govern the pathogenesis of COVID-19.

Publications

Differences in HIV burden and immune activation within the gut of HIV-positive patients receiving suppressive antiretroviral therapy.

The Journal of infectious diseases

Yukl SA, Gianella S, Sinclair E, Epling L, Li Q, Duan L, Choi AL, Girling V, Ho T, Li P, Fujimoto K, Lampiris H, Hare CB, Pandori M, Haase AT, Günthard HF, Fischer M, Shergill AK, McQuaid K, Havlir DV, Wong JK

Effect of raltegravir-containing intensification on HIV burden and T-cell activation in multiple gut sites of HIV-positive adults on suppressive antiretroviral therapy.

AIDS (London, England)

Yukl SA, Shergill AK, McQuaid K, Gianella S, Lampiris H, Hare CB, Pandori M, Sinclair E, Günthard HF, Fischer M, Wong JK, Havlir DV

Challenges in detecting HIV persistence during potentially curative interventions: a study of the Berlin patient.

PLoS pathogens

Yukl SA, Boritz E, Busch M, Bentsen C, Chun TW, Douek D, Eisele E, Haase A, Ho YC, Hütter G, Justement JS, Keating S, Lee TH, Li P, Murray D, Palmer S, Pilcher C, Pillai S, Price RW, Rothenberger M, Schacker T, Siliciano J, Siliciano R, Sinclair E, Strain M, Wong J, Richman D, Deeks SG

HIV latency in isolated patient CD4+ T cells may be due to blocks in HIV transcriptional elongation, completion, and splicing.

Science translational medicine

Yukl SA, Kaiser P, Kim P, Telwatte S, Joshi SK, Vu M, Lampiris H, Wong JK

Gut and blood differ in constitutive blocks to HIV transcription, suggesting tissue-specific differences in the mechanisms that govern HIV latency.

PLoS pathogens

Telwatte S, Lee S, Somsouk M, Hatano H, Baker C, Kaiser P, Kim P, Chen TH, Milush J, Hunt PW, Deeks SG, Wong JK, Yukl SA