Transcomplementation of VIF- HIV-1 Mutants in CEM Cells Suggests That VIF Affects Late Steps of the Viral Life Cycle

Blanc, Dominique; Patience, Olive; Schulz, Thomas F.; Weiss, Robin A.; Spire, Bruno

doi:10.1006/viro.1993.1114

Cited by 57 publications

(67 citation statements)

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“…6A, left panels, Gag VLPs were most abundant in fractions 4 to 6, corresponding to the density of 1.16 to 1.20 g/cm 3 typical for retroviral particles. Detergent treatment of VLPs shifted the Gag signal to fraction 3 with a density of 1.26 g/cm 3 ( Fig. 6A, right panels), consistent with the removal of lipid envelopes.…”

Section: Analysis Of Vif Encapsidation In Gag and Vif Coexpression Symentioning

confidence: 99%

“…6, the Vif signal colocalized with Gag, demonstrating that Vif was specifically incorporated in VLPs. For Gag⌬350-362, the density of untreated VLPs ranged between 1.15 and 1.17 g/cm 3 ( Fig. 8B, top left set of panels, fractions 6 and 7), while the detergent-treated VLPs migrated to fractions with a density of 1.25 to 1.27 g/cm 3 ( Fig.…”

Section: Pattern Of Vif Incorporation In Vlps and Virions Consisting mentioning

confidence: 99%

“…For Gag⌬350-362, the density of untreated VLPs ranged between 1.15 and 1.17 g/cm 3 ( Fig. 8B, top left set of panels, fractions 6 and 7), while the detergent-treated VLPs migrated to fractions with a density of 1.25 to 1.27 g/cm 3 ( Fig. 8B, top right set of panels, fractions 2 and 3), identical to the wild-type Gag VLPs (compare with Fig.…”

Section: Pattern Of Vif Incorporation In Vlps and Virions Consisting mentioning

confidence: 99%

“…In cell culture, vif-defective (vif Ϫ ) HIV-1 is able to replicate in some T-lymphoblastoid cell lines termed permissive (CEM-SS, SupT1, C8166, and Jurkat) whereas Vif is required in other cell lines, such as H9 or MT-2, termed nonpermissive (18,22,37,64,66,69). It is generally accepted that Vif acts in late steps of the viral life cycle to ensure production of infectious virions (3,12,53,56,61,64,69). vif Ϫ HIV-1 is impaired in endogenous reverse transcription and in its ability to form proviral DNA in newly infected cells (4,25,59,64,69).…”

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confidence: 99%

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Vif Is Largely Absent from Human Immunodeficiency Virus Type 1 Mature Virions and Associates Mainly with Viral Particles Containing Unprocessed Gag

Sova

Volsky

Chao

2001

J Virol

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Section: Analysis Of Vif Encapsidation In Gag and Vif Coexpression Symentioning

confidence: 99%

Section: Pattern Of Vif Incorporation In Vlps and Virions Consisting mentioning

confidence: 99%

Section: Pattern Of Vif Incorporation In Vlps and Virions Consisting mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Vif Is Largely Absent from Human Immunodeficiency Virus Type 1 Mature Virions and Associates Mainly with Viral Particles Containing Unprocessed Gag

Sova

Volsky

Chao

2001

J Virol

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“…In non-permissive cells, ⌬vif viruses can produce virions, but they fail to complete reverse transcription and cannot establish infection (10,15,16). The expression of Vif in trans in virus-producing cells but not target cells rescues this defect (17). Vif forms a complex with APOBEC3G, preventing its viral encapsidation, and thereby protects the viral genome from editing mutations (8).…”

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confidence: 99%

Vif Overcomes the Innate Antiviral Activity of APOBEC3G by Promoting Its Degradation in the Ubiquitin-Proteasome Pathway

Mehle

Strack

Ancuța

et al. 2004

Journal of Biological Chemistry

431

380

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Viruses must overcome diverse intracellular defense mechanisms to establish infection. The Vif (virion infectivity factor) protein of human immunodeficiency virus 1 (HIV-1) acts by overcoming the antiviral activity of APOBEC3G (CEM15), a cytidine deaminase that induces G to A hypermutation in newly synthesized viral DNA. In the absence of Vif, APOBEC3G incorporation into virions renders HIV-1 non-infectious. We report here that Vif counteracts the antiviral activity of APOBEC3G by targeting it for destruction by the ubiquitin-proteasome pathway. Vif forms a complex with APOBEC3G and enhances APOBEC3G ubiquitination, resulting in reduced steady-state APOBEC3G levels and a decrease in protein half-life. Furthermore, Vif-dependent degradation of APOBEC3G is blocked by proteasome inhibitors or ubiquitin mutant K48R. A mutation of highly conserved cysteines or the deletion of a conserved SLQ(Y/F)LA motif in Vif results in mutants that fail to induce APOBEC3G degradation and produce non-infectious HIV-1; however, mutations of conserved phosphorylation sites in Vif that impair viral replication do not affect APOBEC3G degradation, suggesting that Vif is important for other functions in addition to inducing proteasomal degradation of APOBEC3G. Vif is monoubiquitinated in the absence of APOBEC3G but is polyubiquitinated and rapidly degraded when APOBEC3G is coexpressed, suggesting that coexpression accelerates the degradation of both proteins. These results suggest that Vif functions by targeting APOBEC3G for degradation via the ubiquitin-proteasome pathway and implicate the proteasome as a site of dynamic interplay between microbial and cellular defenses.

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Prevalence of anti-Vif antibodies in HIV-1 infected individuals assessed using recombinant baculovirus expressedVif protein

et al. 1997

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A 630 base pair fragment of the HIV-1 genome encompassing the entire vif open reading frame has been produced by the polymerase chain reaction and cloned into the baculovirus transfer vector pAcYM1. Extracts from insect cells infected with a recombinant baculovirus expressing the HIV-1 vif gene product were used in a radioimmunoassay to analyse 238 sera from HIV infected individuals for the presence of anti-vif antibodies. The overall prevalence of anti-vif antibodies in this group of patients was 25.3%. Stratification of the group according to CD4 levels showed that anti-vif antibodies were more prevalent in patients with CD4 counts below the median of the group (155 x 10(6) cells/L; P = 0.005). A significant increase in anti-vif antibodies was observed in patients with CD4 levels less than 280 x 10(6) cells/L (P < 0.01) and in patients with symptomatic HIV infection (P = 0.0003). However, there was no significant difference in the prevalence of anti-vif antibodies in patients stratified according to p24 antigen status. The implications of these findings in the context of HIV replication are discussed.

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Transcomplementation of VIF- HIV-1 Mutants in CEM Cells Suggests That VIF Affects Late Steps of the Viral Life Cycle

Cited by 57 publications

References 0 publications

Vif Is Largely Absent from Human Immunodeficiency Virus Type 1 Mature Virions and Associates Mainly with Viral Particles Containing Unprocessed Gag

Vif Is Largely Absent from Human Immunodeficiency Virus Type 1 Mature Virions and Associates Mainly with Viral Particles Containing Unprocessed Gag

Vif Overcomes the Innate Antiviral Activity of APOBEC3G by Promoting Its Degradation in the Ubiquitin-Proteasome Pathway

Prevalence of anti-Vif antibodies in HIV-1 infected individuals assessed using recombinant baculovirus expressedVif protein

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