ArticleJournal of virology2003
Comprehensive investigation of the molecular defect in vif-deficient human immunodeficiency virus type 1 virions.
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 33 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Antagonism of PP2A is an independent and conserved function of HIV-1 Vif and causes cell cycle arrest.eLife · 2020Article
- Deep sequencing of HIV-1 reverse transcripts reveals the multifaceted antiviral functions of APOBEC3G.Nature microbiology · 2018Article
- HIV-1 and M-PMV RNA Nuclear Export Elements Program Viral Genomes for Distinct Cytoplasmic Trafficking Behaviors.PLoS pathogens · 2016Article
- RNA binding to APOBEC3G induces the disassembly of functional deaminase complexes by displacing single-stranded DNA substrates.Nucleic acids research · 2015Article
- The HDAC6/APOBEC3G complex regulates HIV-1 infectiveness by inducing Vif autophagic degradation.Retrovirology · 2015Article
- Promiscuous RNA binding ensures effective encapsidation of APOBEC3 proteins by HIV-1.PLoS pathogens · 2015Article
- Cooperativity among Rev-associated nuclear export signals regulates HIV-1 gene expression and is a determinant of virus species tropism.Journal of virology · 2014Article
- In vivo HIV-1 hypermutation and viral loads among antiretroviral-naive Brazilian patients.AIDS research and human retroviruses · 2014Article
- Endogenous MOV10 inhibits the retrotransposition of endogenous retroelements but not the replication of exogenous retroviruses.Retrovirology · 2012Article
- Evolution of a species-specific determinant within human CRM1 that regulates the post-transcriptional phases of HIV-1 replication.PLoS pathogens · 2011Article
- APOBEC1-mediated editing and attenuation of herpes simplex virus 1 DNA indicate that neurons have an antiviral role during herpes simplex encephalitis.Journal of virology · 2011Article
- APOBEC3G: a double agent in defense.Trends in biochemical sciences · 2011Article
- HIV-1 Vif versus the APOBEC3 cytidine deaminases: an intracellular duel between pathogen and host restriction factors.Molecular aspects of medicine · 2010Review
- SRp40 and SRp55 promote the translation of unspliced human immunodeficiency virus type 1 RNA.Journal of virology · 2010Article
- The antiviral factor APOBEC3G improves CTL recognition of cultured HIV-infected T cells.The Journal of experimental medicine · 2010Article
- Matrix mediates the functional link between human immunodeficiency virus type 1 RNA nuclear export elements and the assembly competency of Gag in murine 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
- Mutational analysis of the HIV-1 auxiliary protein Vif identifies independent domains important for the physical and functional interaction with HIV-1 reverse transcriptase.Nucleic acids research · 2009Article
- APOBEC proteins and intrinsic resistance to HIV-1 infection.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009Review
- Human immunodeficiency virus type-1 reverse transcriptase exists as post-translationally modified forms in virions and cells.Retrovirology · 2008Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Replication of human immunodeficiency virus type 1 (HIV-1) in primary blood lymphocytes, certain T-cell lines (nonpermissive cells), and most likely in vivo is highly dependent on the virally encoded Vif protein. Evidence suggests that Vif acts late in the viral life cycle during assembly, budding, and/or maturation to counteract the antiviral activity of the CEM15 protein and possibly other antiviral factors. Because HIV-1 virions produced in the absence of Vif are severely restricted at a postentry, preintegration step of infection, it is presumed that such virions differ from wild-type virions in some way. In the present study, we established a protocol for producing large quantities of vif-deficient HIV-1 (HIV-1/Delta vif) from an acute infection of nonpermissive T cells and performed a thorough examination of the defect in these virions. Aside from the expected lack of Vif, we observed no apparent abnormalities in the packaging, modification, processing, or function of proteins in Delta vif virions. In addition, we found no consistent defect in the ability of Delta vif virions to perform intravirion reverse transcription under a variety of assay conditions, suggesting that the reverse transcription complexes in these particles can behave normally under cell-free conditions. Consistent with this finding, neither the placement of the primer tRNA3Lys nor its ability to promote reverse transcription in an in vitro assay was affected by a lack of Vif. Based on the inability of this comprehensive analysis to uncover molecular defects in Delta vif virions, we speculate that such defects are likely to be subtle and/or rare.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.