Potent Suppression of Viral Infectivity by the Peptides That Inhibit Multimerization of Human Immunodeficiency Virus Type 1 (HIV-1) Vif Proteins

Yang, Bin; Gao, Ling; Li, Lin; Lu, Zhixian; Fan, Xuejun; Patel, Charvi; Pomerantz, Roger J.; Dubois, Garrett C.; Zhang, Hui

doi:10.1074/jbc.m210164200

Cited by 75 publications

(83 citation statements)

References 34 publications

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“…In particular, a 15-mer containing the amino-acid sequence motif PPLP was found to be significant for inhibiting Vif multimerization. More importantly, these peptides strongly inhibited HIV-1 replication in nonpermissive H9-cells, 17 showing their broad utility.…”

Section: Dominant-negative Effectors Against Hiv-1 Inhibit Viral Replmentioning

confidence: 94%

“…This protein appears to interact with the HIV-1 Gag polyprotein P55Gag; this seems to drive the efficiency of infectivity of progeny virions by modulating assembly, budding, and/or maturation. Disrupting Vif assembly is an attractive target for gene therapy and several published studies 16,17 are aimed at finding peptides that in a transdominant negative manner disrupt its oligomerization. In one study, a 12-mer containing the aminoacid sequence PXP motif, proline-X-proline, identified through phage display, inhibited Vif oligomerization in vitro.…”

Section: Dominant-negative Effectors Against Hiv-1 Inhibit Viral Replmentioning

confidence: 99%

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Gene therapy progress and prospects: Novel gene therapy approaches for AIDS

Wolkowicz

Nolan

2005

Gene Ther

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Section: Dominant-negative Effectors Against Hiv-1 Inhibit Viral Replmentioning

confidence: 94%

Section: Dominant-negative Effectors Against Hiv-1 Inhibit Viral Replmentioning

confidence: 99%

Gene therapy progress and prospects: Novel gene therapy approaches for AIDS

Wolkowicz

Nolan

2005

Gene Ther

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“…Vif tryptophan residues 5, 11, 21, and 38, involved in APOBEC3G antagonism, were completely conserved among transmitted viruses, nor was there any variation in the 144-SLQYLA-149 motif, supporting Vif anti-APOBEC3G function as critical during early infection. [42][43][44][45][46][47][48][49] Despite previous reports of low sequence variability, 36 Vif amino acid residues 63-70, required for the formation of b-strand structures and critical in maintaining normal vif expression levels, 50 showed slight variations in the t/f viruses to a similar degree as those published in the extended subtype C consensus 51 ; therefore, the presence of the weak basic amino acid Gln in place of acidic Glu may not affect steady-state expression. The 90-RLRR-93 motif was not conserved in the transmitted viruses similar to previously reported subtype C analyses.…”

Section: Discussionmentioning

confidence: 54%

Transmitted/Founder HIV-1 Subtype C Viruses Show Distinctive Signature Patterns in Vif, Vpr, and Vpu That Are Under Subsequent Immune Pressure During Early Infection

Rossenkhan

MacLeod

Brumme

et al. 2016

AIDS Research and Human Retroviruses

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Viral variants that predominate during early infection may exhibit constrained diversity compared with those found during chronic infection and could contain amino acid signature patterns that may enhance transmission, establish productive infection, and influence early events that modulate the infection course. We compared amino acid distributions in 17 patients recently infected with HIV-1C with patients with chronic infection. We found significantly lower entropy in inferred transmitted/founder (t/f) compared with chronic viruses and identified signature patterns in Vif and Vpr from inferred t/f viruses. We investigated sequence evolution longitudinally up to 500 days postseroconversion and compared the impact of selected substitutions on predicted human leukocyte antigen (HLA) binding affinities of published and predicted cytotoxic T-lymphocyte epitopes. Polymorphisms in Vif and Vpr during early infection occurred more frequently at epitope-HLA anchor residues and significantly decreased predicted epitope-HLA binding. Transmission-associated sequence signatures may have implications for novel strategies to prevent HIV-1 transmission.

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“…1). This region, which is proteolytically processed in virion-associated Vif (119), is involved in Pr55 Gag interactions (24) and Vif self-association and multimerization (250,251) (Fig. 1).…”

Section: Pivotal Role For the C-terminal Tail Of Vifmentioning

confidence: 99%

“…1). Multimerization may be required for cooperative binding to RNA (14,89) and pathogenesis (250), since a deletion of the multimerization domain (161PPLP164) impaired viral infectivity in H9 cells (251), and a Vif dimerization antagonist peptide suppresses HIV-1 infectivity (158). Mass spectroscopy analysis revealed an increase in the ordered structure of the C-terminal domain upon Vif oligomerization (8).…”

Section: Pivotal Role For the C-terminal Tail Of Vifmentioning

confidence: 99%

Tumultuous Relationship between the Human Immunodeficiency Virus Type 1 Viral Infectivity Factor (Vif) and the Human APOBEC-3G and APOBEC-3F Restriction Factors

Henriet

Mercenne

Bernacchi

et al. 2009

Microbiol Mol Biol Rev

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SUMMARY The viral infectivity factor (Vif) is dispensable for human immunodeficiency virus type 1 (HIV-1) replication in so-called permissive cells but is required for replication in nonpermissive cell lines and for pathogenesis. Virions produced in the absence of Vif have an aberrant morphology and an unstable core and are unable to complete reverse transcription. Recent studies demonstrated that human APOBEC-3G (hA3G) and APOBEC-3F (hA3F), which are selectively expressed in nonpermissive cells, possess strong anti-HIV-1 activity and are sufficient to confer a nonpermissive phenotype. Vif induces the degradation of hA3G and hA3F, suggesting that its main function is to counteract these cellular factors. Most studies focused on the hypermutation induced by the cytidine deaminase activity of hA3G and hA3F and on their Vif-induced degradation by the proteasome. However, recent studies suggested that several mechanisms are involved both in the antiviral activity of hA3G and hA3F and in the way Vif counteracts these antiviral factors. Attempts to reconcile the studies involving Vif in virus assembly and stability with these recent findings suggest that hA3G and hA3F partially exert their antiviral activity independently of their catalytic activity by destabilizing the viral core and the reverse transcription complex, possibly by interfering with the assembly and/or maturation of the viral particles. Vif could then counteract hA3G and hA3F by excluding them from the viral assembly intermediates through competition for the viral genomic RNA, by regulating the proteolytic processing of Pr55Gag, by enhancing the efficiency of the reverse transcription process, and by inhibiting the enzymatic activities of hA3G and hA3F.

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Potent Suppression of Viral Infectivity by the Peptides That Inhibit Multimerization of Human Immunodeficiency Virus Type 1 (HIV-1) Vif Proteins

Cited by 75 publications

References 34 publications

Gene therapy progress and prospects: Novel gene therapy approaches for AIDS

Gene therapy progress and prospects: Novel gene therapy approaches for AIDS

Transmitted/Founder HIV-1 Subtype C Viruses Show Distinctive Signature Patterns in Vif, Vpr, and Vpu That Are Under Subsequent Immune Pressure During Early Infection

Tumultuous Relationship between the Human Immunodeficiency Virus Type 1 Viral Infectivity Factor (Vif) and the Human APOBEC-3G and APOBEC-3F Restriction Factors

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