ArticleJournal of virology2008
Species-specific restriction of apobec3-mediated hypermutation.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 78 citations in OpenAlex.
- A Viral Protein Antagonist for Both AID and APOBEC3.Viruses · 2026Review
- Article
- DHX15 inhibits mouse APOBEC3 deamination.PLoS pathogens · 2025Article
- Myelodysplasia after clonal hematopoiesis with APOBEC3-mediated CYBB inactivation in retroviral gene therapy for X-CGD.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- CoelacanthJournal of virology · 2021Article
- Deaminase-Independent Mode of Antiretroviral Action in Human and Mouse APOBEC3 Proteins.Microorganisms · 2020Review
- The Role of APOBECs in Viral Replication.Microorganisms · 2020Review
- Mouse APOBEC3 Restriction of Retroviruses.Viruses · 2020Review
- Mouse APOBEC3 interferes with autocatalytic cleavage of murine leukemia virus Pr180gag-pol precursor and inhibits Pr65gag processing.PLoS pathogens · 2019Article
- Friend retrovirus studies reveal complex interactions between intrinsic, innate and adaptive immunity.FEMS microbiology reviews · 2019Review
- Review
- Therapeutic activity of retroviral replicating vector-mediated prodrug activator gene therapy for pancreatic cancer.Cancer gene therapy · 2018Article
- Deaminase-Dead Mouse APOBEC3 Is anJournal of virology · 2018Article
- Mouse APOBEC3 expression in NIH 3T3 cells mediates hypermutation of AKV murine leukemia virus.Virology · 2018Article
- Full-Length Glycosylated Gag of Murine Leukemia Virus Can Associate with the Viral Envelope as a Type I Integral Membrane Protein.Journal of virology · 2018Article
- Restriction Factors: From Intrinsic Viral Restriction to Shaping Cellular Immunity Against HIV-1.Frontiers in immunology · 2018Review
- How Active Are Porcine Endogenous Retroviruses (PERVs)?Viruses · 2016Review
- The interferon-induced antiviral protein PML (TRIM19) promotes the restriction and transcriptional silencing of lentiviruses in a context-specific, isoform-specific fashion.Retrovirology · 2016Article
- Human and murine APOBEC3s restrict replication of koala retrovirus by different mechanisms.Retrovirology · 2015Article
- N-linked glycosylation protects gammaretroviruses against deamination by APOBEC3 proteins.Journal of virology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Apobec proteins are a family of cellular cytidine deaminases, among which several members have been shown to have potent antiviral properties. This antiviral activity is associated with the ability to cause hypermutation of retroviral cDNA. However, recent research has indicated that Apobec proteins are also able to inhibit retroviruses by other mechanisms that are independent of their deaminase activity. We have compared the antiviral activities of human and murine Apobec3 (A3) proteins, and we have found that, consistent with previous reports, human immunodeficiency virus (HIV) is able to resist human A3G but is sensitive to murine A3, whereas murine leukemia virus (MLV) is relatively resistant to murine A3 (mA3) but sensitive to human A3G. In contrast to previous studies, we observed that mA3 is packaged efficiently into MLV particles. The C-terminal cytidine deaminase domain (CDD2) is required for packaging of mA3 into MLV particles, and packaging did not depend on the MLV viral RNA. However, mA3 packed into MLV particles failed to cause hypermutation of viral DNA, indicating that its deaminase activity is blocked or inhibited. hA3G also caused significantly less hypermutation of MLV than of HIV DNA. Both mA3 and the splice variant mA3Delta5 exhibited some residual antiviral activity against MLV and caused a reduction in the ability of MLV particles to generate reverse transcription products. These results suggest that MLV has evolved specific mechanisms to block the ability of Apobec proteins to mediate deaminase-dependent hypermutation.
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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.