ReviewViruses2012
Running loose or getting lost: how HIV-1 counters and capitalizes on APOBEC3-induced mutagenesis through its Vif protein.
Review in Viruses, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed.
- APOBEC3G Antagonism by Vif, or When Structure Meets Biological and Evolutionary Studies.Annual review of virology · 2025Review
- Shaping the regulation of the p53 mRNA tumour suppressor: the co-evolution of genetic signatures.BMC cancer · 2019Review
- In Vivo Examination of Mouse APOBEC3- and Human APOBEC3A- and APOBEC3G-Mediated Restriction of Parvovirus and Herpesvirus Infection in Mouse Models.Journal of virology · 2016Article
- The effect of HIV-1 Vif polymorphisms on A3G anti-viral activity in an in vivo mouse model.Retrovirology · 2016Article
- APOBEC4 Enhances the Replication of HIV-1.PloS one · 2016Article
- APOBEC3 Proteins in Viral Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2015Review
- The Road Less Traveled: HIV's Use of Alternative Routes through Cellular Pathways.Journal of virology · 2015Review
- Review
- A functional conserved intronic G run in HIV-1 intron 3 is critical to counteract APOBEC3G-mediated host restriction.Retrovirology · 2014Article
- Prototype foamy virus Bet impairs the dimerization and cytosolic solubility of human APOBEC3G.Journal of virology · 2013Article
- Identification of the feline foamy virus Bet domain essential for APOBEC3 counteraction.Retrovirology · 2013Article
- The role of cytidine deaminases on innate immune responses against human viral infections.BioMed research international · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human immunodeficiency virus-1 (HIV-1) dynamics reflect an intricate balance within the viruses’ host. The virus relies on host replication factors, but must escape or counter its host’s antiviral restriction factors. The interaction between the HIV-1 protein Vif and many cellular restriction factors from the APOBEC3 protein family is a prominent example of this evolutionary arms race. The viral infectivity factor (Vif) protein largely neutralizes APOBEC3 proteins, which can induce in vivo hypermutations in HIV-1 to the extent of lethal mutagenesis, and ensures the production of viable virus particles. HIV-1 also uses the APOBEC3-Vif interaction to modulate its own mutation rate in harsh or variable environments, and it is a model of adaptation in a coevolutionary setting. Both experimental evidence and the substantiation of the underlying dynamics through coevolutionary models are presented as complementary views of a coevolutionary arms race.
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What OpenQuestion holds
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.