BRD9 functions as an HIV-1 latency regulatory factor

T Tsz-Yat Luk (AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong) L Lok-Yan Yim (AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong) R Runhong Zhou (AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong) Y Yufei Mo (AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong) H Huarong Huang (AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong) M Meiqing Zhao (AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong) J Jie Dai (State Key Laboratory of Green Papermaking and Resource Recycling, School of Environmental Science and Engineering) T Thomas Tsz-Kan Lau (AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong) X Xiner Huang (Department of Microbiology, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong) G Grace Chung-Yan Lui (Division of Infectious Diseases, Department of Medicine and Therapeutics, The Chinese University of Hong Kong) K Kwok-Yung Yuen (Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong) J Jasper Fuk-Woo Chan (Department of Microbiology, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong) A Alfred Sze-Lok Cheng (School of Biomedical Sciences, The Chinese University of Hong Kong) Z Zhiwei Chen H Hin Chu (Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong)

Abstract

A major challenge for HIV type 1 (HIV-1) cure is the presence of viral latent reservoirs. The “Shock & Kill” strategy involves the combined use of latency reversal agents (LRA) and antiretroviral treatment (ART) to reactivate HIV-1 latent reservoirs, followed by elimination of infected cells. However, current LRAs are insufficient in fully reactivating the latent reservoirs. Therefore, investigation on novel HIV-1 latency regulators will be crucial to the success of HIV-1 cure research. Here, we identify bromodomain-containing protein 9 (BRD9) as an HIV-1 latency regulator. BRD9 inhibition induces HIV-1 latency reactivation in T cell lines, human resting memory CD4 + T cells, and PBMCs derived from people living with HIV-1 (PWH) on ART. BRD9 inhibition, gene depletion, and protein degradation consistently reactivate HIV-1 latency. Moreover, BRD9 inhibition synergizes with BRD4 inhibition in inducing HIV-1 production. Mechanistically, BRD9 binds to HIV-1 LTR promoter and competes with HIV-1 Tat protein for binding to the HIV-1 genome. Additionally, our integrated CUT&RUN DNA sequencing, transcriptomics, and pharmacological analysis revealed downstream host targets of BRD9, including ATAD2 and MTHFD2, that modulate HIV-1 latency.

Article Details

Volume / Issue Vol. 122, Issue 21
Published May 27, 2025
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (15)

T

Tsz-Yat Luk

AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong

L

Lok-Yan Yim

AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong

R

Runhong Zhou

AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong

Y

Yufei Mo

AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong

H

Huarong Huang

AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong

M

Meiqing Zhao

AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong

J

Jie Dai

State Key Laboratory of Green Papermaking and Resource Recycling, School of Environmental Science and Engineering

T

Thomas Tsz-Kan Lau

AIDS Institute, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong

X

Xiner Huang

Department of Microbiology, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong

G

Grace Chung-Yan Lui

Division of Infectious Diseases, Department of Medicine and Therapeutics, The Chinese University of Hong Kong

K

Kwok-Yung Yuen

Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong

J

Jasper Fuk-Woo Chan

Department of Microbiology, School of Clinical Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong

A

Alfred Sze-Lok Cheng

School of Biomedical Sciences, The Chinese University of Hong Kong

Z

Zhiwei Chen

H

Hin Chu

Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong