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The interaction of APOBEC3G with human immunodeficiency virus type 1 nucleocapsid inhibits tRNA3Lys annealing to viral RNA
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Identification of two distinct human immunodeficiency virus type 1 Vif determinants critical for interactions with human APOBEC3G and APOBEC3F
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Human immunodeficiency virus type 1 cDNAs produced in the presence of APOBEC3G exhibit defects in plus-strand DNA transfer and integration
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Cytidine deaminases APOBEC3G and APOBEC3F interact with human immunodeficiency virus type 1 integrase and inhibit proviral DNA formation
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APOBEC-mediated viral restriction: not simply editing?
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Identification of APOBEC3DE as another antiretroviral factor from the human APOBEC family
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Population level analysis of human immunodeficiency virus type 1 hypermutation and its relationship with APOBEC3G and vif genetic variation
Craig Pace et al.
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A zinc-binding region in vif binds cul5 and determines cullin selection
Andrew Mehle et al.
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Differential requirement for conserved tryptophans in human immunodeficiency virus type 1 Vif for the selective suppression of APOBEC3G and APOBEC3F
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Role and mechanism of action of the APOBEC3 family of antiretroviral resistance factors
BR Cullen
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Natural variation in Vif: Differential impact on APOBEC3G/3F and a potential role in HIV-1 diversification
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G→A hypermutation in protease and reverse transcriptase regions of human immunodeficiency virus type 1 residing in resting CD4+ T cells in vivo
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Vif overcomes the innate antiviral activity of APOBEC3G by promoting its degradation in the ubiquitin-proteasome pathway
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Biased G-to-A hypermutation in HIV-1 proviral DNA from a long-term non-progressor
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APOBEC3F properties and hypermutation preferences indicate activity against HIV-1 in vivo
MT Liddament et al.
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Antiretroviral drug resistance mutations in human immunodeficiency virus type 1 reverse transcriptase increase template-switching frequency
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A second human antiretroviral factor, APOBEC3F, is suppressed by the HIV-1 and HIV-2 Vif proteins
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Human APOBEC3F is another host factor that blocks human immunodeficiency virus type 1 replication
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Intrinsic immunity: a front-line defense against viral attack
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Single-strand specificity of APOBEC3G accounts for minus-strand deamination of the HIV genome
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Hypermutation of HIV type 1 genomes isolated from infants soon after vertical infection
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HIV-1 Vif protein binds the editing enzyme APOBEC3G and induces its degradation
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The human immunodeficiency virus type 1 Vif protein reduces intracellular expression and inhibits packaging of APOBEC3G (CEM15), a cellular inhibitor of virus infectivity
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Recombination - Multiply infected spleen cells in HIV patients
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Human immunodeficiency virus type 1 DNA sequences genetically damaged by hypermutation are often abundant in patient peripheral blood mononuclear cells and may be generated during near-simultaneous infection and activation of CD4+ T cells
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