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Title: HIV-1 accessory proteins VPR and Vif modulate antiviral response by targeting IRF-3 for degradation

Journal Article · · Virology
; ;  [1];  [2];  [3];  [4]
  1. The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21231 (United States)
  2. University of Maryland, School of Medicine, Baltimore, MD 21231 (United States)
  3. Laboratory of Molecular Microbiology, National Institutes of Health, Bethesda, MD 20892 (United States)
  4. Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University, Baltimore, MD 21231 (United States)

The activation of IRF-3 during the early stages of viral infection is critical for the initiation of the antiviral response; however the activation of IRF-3 in HIV-1 infected cells has not yet been characterized. We demonstrate that the early steps of HIV-1 infection do not lead to the activation and nuclear translocation of IRF-3; instead, the relative levels of IRF-3 protein are decreased due to the ubiquitin-associated proteosome degradation. Addressing the molecular mechanism of this effect we show that the degradation is independent of HIV-1 replication and that virion-associated accessory proteins Vif and Vpr can independently degrade IRF-3. The null mutation of these two genes reduced the capacity of the HIV-1 virus to down modulate IRF-3 levels. The degradation was associated with Vif- and Vpr-mediated ubiquitination of IRF-3 and was independent of the activation of IRF-3. N-terminal lysine residues were shown to play a critical role in the Vif- and Vpr-mediated degradation of IRF-3. These data implicate Vif and Vpr in the disruption of the initial antiviral response and point to the need of HIV-1 to circumvent the antiviral response during the very early phase of replication.

OSTI ID:
21078035
Journal Information:
Virology, Vol. 373, Issue 1; Other Information: DOI: 10.1016/j.virol.2007.10.042; PII: S0042-6822(07)00732-5; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0042-6822
Country of Publication:
United States
Language:
English