ArticleJournal of virology2010
Stably expressed APOBEC3F has negligible antiviral activity.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
- Dodging the Host Interferon-Stimulated Gene Mediated Innate Immunity by HIV-1: A Brief Update on Intrinsic Mechanisms and Counter-Mechanisms.Frontiers in immunology · 2021Review
- Article
- Long-term passage of Vif-null HIV-1 in CD4Virology · 2017Article
- Correlation of Apobec Mrna Expression with overall Survival and pd-l1 Expression in Urothelial Carcinoma.Scientific reports · 2016Article
- 1.92 Angstrom Zinc-Free APOBEC3F Catalytic Domain Crystal Structure.Journal of molecular biology · 2016Article
- Role of APOBEC3F Gene Variation in HIV-1 Disease Progression and Pneumocystis Pneumonia.PLoS genetics · 2016Article
- Anti-APOBEC3G activity of HIV-1 Vif protein is attenuated in elite controllers.Journal of virology · 2015Article
- Correlation of APOBEC3 in tumor tissues with clinico-pathological features and survival from hepatocellular carcinoma after curative hepatectomy.International journal of clinical and experimental medicine · 2015Article
- Possible footprints of APOBEC3F and/or other APOBEC3 deaminases, but not APOBEC3G, on HIV-1 from patients with acute/early and chronic infections.Journal of virology · 2014Article
- APOBEC3D and APOBEC3F potently promote HIV-1 diversification and evolution in humanized mouse model.PLoS pathogens · 2014Article
- HIV-1 and HIV-2 Vif interact with human APOBEC3 proteins using completely different determinants.Journal of virology · 2014Article
- Multiple APOBEC3 restriction factors for HIV-1 and one Vif to rule them all.Journal of molecular biology · 2014Review
- Different mutagenic potential of HIV-1 restriction factors APOBEC3G and APOBEC3F is determined by distinct single-stranded DNA scanning mechanisms.PLoS pathogens · 2014Article
- Catalytic activity of APOBEC3F is required for efficient restriction of Vif-deficient human immunodeficiency virus.Virology · 2014Article
- Article
- Article
- Suppression of APOBEC3-mediated restriction of HIV-1 by Vif.Frontiers in microbiology · 2014Review
- HIV restriction by APOBEC3 in humanized mice.PLoS pathogens · 2013Article
- IFN-α treatment inhibits acute Friend retrovirus replication primarily through the antiviral effector molecule Apobec3.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
APOBEC3F (A3F) is a member of the family of cytidine deaminases that is often coexpressed with APOBEC3G (A3G) in cells susceptible to HIV infection. A3F has been shown to have strong antiviral activity in transient-expression studies, and together with A3G, it is considered the most potent cytidine deaminase targeting HIV. Previous analyses suggested that the antiviral properties of A3F can be dissociated from its catalytic deaminase activity. We were able to confirm the deaminase-independent antiviral activity of exogenously expressed A3F; however, we also noted that exogenous expression was associated with very high A3F mRNA and protein levels. In analogy to our previous study of A3G, we produced stable HeLa cell lines constitutively expressing wild-type or deaminase-defective A3F at levels that were more in line with the levels of endogenous A3F in H9 cells. A3F expressed in stable HeLa cells was packaged into Vif-deficient viral particles with an efficiency similar to that of A3G and was properly targeted to the viral nucleoprotein complex. Surprisingly, however, neither wild-type nor deaminase-defective A3F inhibited HIV-1 infectivity. These results imply that the antiviral activity of endogenous A3F is negligible compared to that of A3G.
Indexed as
Identifiers
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.