ArticleJournal of virology2003
Human immunodeficiency virus type 1 Vif is efficiently packaged into virions during productive but not chronic infection.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed.
- Review
- A novel HIV-1 inhibitor that blocks viral replication and rescues APOBEC3s by interrupting vif/CBFβ interaction.The Journal of biological chemistry · 2020Article
- Role of the Ubiquitin Proteasome System (UPS) in the HIV-1 Life Cycle.International journal of molecular sciences · 2019Review
- Enterovirus 71 antagonizes the inhibition of the host intrinsic antiviral factor A3G.Nucleic acids research · 2018Article
- Proteasomal Degradation Machinery: Favorite Target of HIV-1 Proteins.Frontiers in microbiology · 2018Review
- Evasion of adaptive immunity by HIV through the action of host APOBEC3G/F enzymes.AIDS research and therapy · 2017Review
- Conserved Interaction of Lentiviral Vif Molecules with HIV-1 Gag and Differential Effects of Species-Specific Vif on Virus Production.Journal of virology · 2017Article
- HIV-1 viral infectivity factor (Vif) alters processive single-stranded DNA scanning of the retroviral restriction factor APOBEC3G.The Journal of biological chemistry · 2013Article
- Article
- Small-molecule inhibition of human immunodeficiency virus type 1 replication by targeting the interaction between Vif and ElonginC.Journal of virology · 2012Article
- Emerging complexities of APOBEC3G action on immunity and viral fitness during HIV infection and treatment.Retrovirology · 2012Review
- Protein intrinsic disorder as a flexible armor and a weapon of HIV-1.Cellular and molecular life sciences : CMLS · 2012Review
- Multifaceted counter-APOBEC3G mechanisms employed by HIV-1 Vif.Journal of molecular biology · 2011Article
- Vif substitution enables persistent infection of pig-tailed macaques by human immunodeficiency virus type 1.Journal of virology · 2011Article
- Identification of dominant negative human immunodeficiency virus type 1 Vif mutants that interfere with the functional inactivation of APOBEC3G by virus-encoded Vif.Journal of virology · 2010Article
- HIV-1 Vif binds to APOBEC3G mRNA and inhibits its translation.Nucleic acids research · 2010Article
- Development of a human immunodeficiency virus type 1-based lentiviral vector that allows efficient transduction of both human and rhesus blood cells.Journal of virology · 2009Article
- Tumultuous relationship between the human immunodeficiency virus type 1 viral infectivity factor (Vif) and the human APOBEC-3G and APOBEC-3F restriction factors.Microbiology and molecular biology reviews : MMBR · 2009Review
- Regulation of Vif mRNA splicing by human immunodeficiency virus type 1 requires 5' splice site D2 and an exonic splicing enhancer to counteract cellular restriction factor APOBEC3G.Journal of virology · 2009Article
- HIV-1 Vif, APOBEC, and intrinsic immunity.Retrovirology · 2008Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Packaging of the human immunodeficiency virus type 1 Vif protein into virus particles is mediated through an interaction with viral genomic RNA and results in the association of Vif with the nucleoprotein complex. Despite the specificity of this process, calculations of the amount of Vif packaged have produced vastly different results. Here, we compared the efficiency of packaging of Vif into virions derived from acutely and chronically infected H9 cells. We found that Vif was efficiently packaged into virions from acutely infected cells (60 to 100 copies per virion), while packaging into virions from chronically infected H9 cells was near the limit of detection (four to six copies of Vif per virion). Superinfection by an exogenous Vif-defective virus did not rescue packaging of endogenous Vif expressed in the chronically infected culture. In contrast, exogenous Vif expressed by superinfection of wild-type virus was readily packaged (30 to 40 copies per virion). Biochemical analyses suggest that the differences in the relative packaging efficiencies were not due to gross differences in the steady-state distribution of Vif in chronically or acutely infected cells but are likely due to differences in the relative rates of de novo synthesis of Vif. Despite its low packaging efficiency, endogenously expressed Vif was sufficient to direct the production of viruses with almost wild-type infectivity. The results from our study provide novel insights into the biochemical properties of Vif and offer an explanation for the reported differences regarding Vif packaging.
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