ArticleRetrovirology2004
HIV-1 Vif and APOBEC3G: multiple roads to one goal.
Article in Retrovirology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
10 citing papers in PubMed, 34 citations in OpenAlex.
- APOBEC3B Potently Restricts HIV-2 but Not HIV-1 in a Vif-Dependent Manner.Journal of virology · 2021Article
- Post-translational Modification-Based Regulation of HIV Replication.Frontiers in microbiology · 2018Review
- Evasion of adaptive immunity by HIV through the action of host APOBEC3G/F enzymes.AIDS research and therapy · 2017Review
- A Novel Regulator of Activation-Induced Cytidine Deaminase/APOBECs in Immunity and Cancer: Schrödinger's CATalytic Pocket.Frontiers in immunology · 2017Review
- Development of Lentiviral Vectors Simultaneously Expressing Multiple siRNAs Against CCR5, vif and tat/rev Genes for an HIV-1 Gene Therapy Approach.Molecular therapy. Nucleic acids · 2016Article
- Review
- Emerging complexities of APOBEC3G action on immunity and viral fitness during HIV infection and treatment.Retrovirology · 2012Review
- On the solution conformation and dynamics of the HIV-1 viral infectivity factor.Journal of molecular biology · 2011Article
- The dimerization domain of HIV-1 viral infectivity factor Vif is required to block virion incorporation of APOBEC3G.Retrovirology · 2007Article
- Feline lentivirus evolution in cross-species infection reveals extensive G-to-A mutation and selection on key residues in the viral polymerase.Journal of virology · 2006Article
Corrections and comments
- Comment on
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The viral infectivity factor, Vif, of human immunodeficiency virus type 1, HIV-1, has long been shown to promote viral replication in vivo and to serve a critical function for productive infection of non-permissive cells, like peripheral blood mononuclear cells (PBMC). Vif functions to counteract an anti-retroviral cellular factor in non-permissive cells named APOBEC3G. The current mechanism proposed for protection of the virus by HIV-1 Vif is to induce APOBEC3G degradation through a ubiquitination-dependent proteasomal pathway. However, a new study published in Retrovirology by Strebel and colleagues suggests that Vif-induced APOBEC3G destruction may not be required for Vif's virus-protective effect. Strebel and co-workers show that Vif and APOBEC3G can stably co-exist, and yet viruses produced under such conditions are fully infectious. This new result highlights the notion that depletion of APOBEC3G is not the sole protective mechanism of Vif and that additional mechanisms exerted by this protein can be envisioned which counteract APOBEC3G and enhance HIV infectivity.
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Identifiers
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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.