Reassessing APOBEC3G Inhibition by HIV-1 Vif-Derived Peptides
نویسندگان
چکیده
منابع مشابه
HIV-1 subtype variability in Vif derived from molecular clones affects APOBEC3G-mediated host restriction.
BACKGROUND The host protein APOBEC3G (A3G) can limit HIV-1 replication. Its protective effect is overcome by the HIV-1 'viral infectivity factor' (Vif), which targets A3G for proteosomal degradation. Although Vif is considered to be essential for HIV-1 replication, the effect of Vif variability among commonly used HIV-1 molecular clones of different genetic backgrounds on viral infectiousness a...
متن کاملDifferential anti-APOBEC3G activity of HIV-1 Vif proteins derived from different subtypes.
Antiretroviral cytidine deaminase APOBEC3G, which is abundantly expressed in peripheral blood lymphocytes and macrophages, strongly protects these cells against HIV-1 infection. The HIV-1 Vif protein overcomes this antiviral effect by enhancing proteasome-mediated APOBEC3G degradation and is key for maintaining viral infectivity. The 579-bp-long vif gene displays high genetic diversity among HI...
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APOBEC3G (A3G), a host protein that inhibits HIV-1 reverse transcription and replication in the absence of Vif, displays cytidine deaminase and single-stranded (ss) nucleic acid binding activities. HIV-1 nucleocapsid protein (NC) also binds nucleic acids and has a unique property, nucleic acid chaperone activity, which is crucial for efficient reverse transcription. Here we report the interplay...
متن کاملASK1 restores the antiviral activity of APOBEC3G by disrupting HIV-1 Vif-mediated counteraction
APOBEC3G (A3G) is an innate antiviral restriction factor that strongly inhibits the replication of human immunodeficiency virus type 1 (HIV-1). An HIV-1 accessory protein, Vif, hijacks the host ubiquitin-proteasome system to execute A3G degradation. Identification of the host pathways that obstruct the action of Vif could provide a new strategy for blocking viral replication. We demonstrate her...
متن کاملSpecies-Specific Exclusion of APOBEC3G from HIV-1 Virions by Vif
The HIV-1 accessory protein Vif (virion infectivity factor) is required for the production of infectious virions by CD4(+) lymphocytes. Vif facilitates particle infectivity by blocking the inhibitory activity of APOBEC3G (CEM15), a virion-encapsidated cellular protein that deaminates minus-strand reverse transcript cytosines to uracils. We report that HIV-1 Vif forms a complex with human APOBEC...
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ژورنال
عنوان ژورنال: Journal of Molecular Biology
سال: 2017
ISSN: 0022-2836
DOI: 10.1016/j.jmb.2016.11.012