Journal of Jilin University(Medicine Edition) ›› 2026, Vol. 52 ›› Issue (5): 1503-1511.doi: 10.13481/j.1671-587X.20260532

• Review • Previous Articles    

Research progress in mechanism of deubiquitinating enzymes in HIV infection

Xue ZHANG,Guangquan LI()   

  1. Research Center,Second Hospital,Jilin University,Changchun 130061,China
  • Received:2025-02-10 Accepted:2025-03-31 Online:2026-09-28 Published:2026-10-15
  • Contact: Guangquan LI E-mail:liguangquan@jlu.edu.cn

Abstract:

Deubiquitinating enzymes (DUBs) play crucial roles in maintaining cellular homeostasis and regulating virus-host interactions by modulating the ubiquitinated status of proteins. During human immunodeficiency virus (HIV) infection, DUBs participate in multiple critical stages of the viral lifecycle, including viral transcription, replication, regulation of host restriction factor stability, and immune evasion, demonstrating their antiviral potential. By regulating key HIV-related molecules, DUBs can directly or indirectly influence HIV replication and dissemination, thereby representing important potential targets for antiviral therapy. However, the DUBs family comprises numerous members with complex functions, and its regulatory network interacts with other post-translational modifications, posing challenges for drug development targeting DUBs. This article systematically reviewed the mechanisms of DUBs in HIV infection, with a focus on their regulation of host restriction factors and key viral proteins, and discussed the significance and potential value of developing novel antiviral drugs targeting DUBs. Through an in-depth analysis of the mechanism of DUBs and the integration of new drug development technologies, it is anticipated that efficient and precise DUB-targeted therapeutic strategies can be achieved, providing new insights and theoretical support for HIV treatment and interventions against other viral infections.

Key words: Ubiquitination, Deubiquitinating enzymes, Human immunodeficiency virus, Antiviral therapy, Autophagy, Gene transcription

CLC Number: 

  • R373.9