ArticleJournal of virology2004
Human APOBEC3F is another host factor that blocks human immunodeficiency virus type 1 replication.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 272 papers, 1 of them a synthesis that pooled it.
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
272 citing papers in PubMed, 1 synthesis or guideline pooled it, 429 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
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- HIV-1 Vif and Vpr cooperatively modulate the cell cycle to maximize per-cell virion production.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- APOBEC3G Antagonism by Vif, or When Structure Meets Biological and Evolutionary Studies.Annual review of virology · 2025Review
- Structural insights into PPP2R5A degradation by HIV-1 Vif.Nature structural & molecular biology · 2024Article
- The Intricate Interplay between APOBEC3 Proteins and DNA Tumour Viruses.Pathogens (Basel, Switzerland) · 2024Review
- Article
- APOBEC3 degradation is the primary function of HIV-1 Vif for virus replication in the myeloid cell line THP-1.bioRxiv : the preprint server for biology · 2023Article
- In-depth investigation of the point mutation pattern of HIV-1.Frontiers in cellular and infection microbiology · 2022Article
- APOBEC3F expression in triple-negative breast cancer is associated with tumor microenvironment infiltration and activation of cancer immunity and improved survival.American journal of cancer research · 2022Article
- APOBEC3B Potently Restricts HIV-2 but Not HIV-1 in a Vif-Dependent Manner.Journal of virology · 2021Article
- Repair of APOBEC3G-Mutated Retroviral DNAJournal of virology · 2021Article
- Elucidation of the Complicated Scenario of Primate APOBEC3 Gene Evolution.Journal of virology · 2021Article
- Foamy Viruses, Bet, and APOBEC3 Restriction.Viruses · 2021Review
- Review
- Retroviral Restriction Factors and Their Viral Targets: Restriction Strategies and Evolutionary Adaptations.Microorganisms · 2020Review
- Crystal Structure of a Soluble APOBEC3G Variant Suggests ssDNA to Bind in a Channel that Extends between the Two Domains.Journal of molecular biology · 2020Article
- Host Immune Response Driving SARS-CoV-2 Evolution.Viruses · 2020Article
- Review
- Deamination hotspots among APOBEC3 family members are defined by both target site sequence context and ssDNA secondary structure.Nucleic acids research · 2020Article
212 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, APOBEC3G has been identified as a host factor that blocks retroviral replication. It introduces G to A hypermutations in newly synthesized minus strand viral cDNA at the step of reverse transcription in target cells. Here, we identified the human APOBEC3F protein as another host factor that blocks human immunodeficiency virus type 1 (HIV-1) replication. Similar to APOBEC3G, APOBEC3F also induced G to A hypermutations in HIV genomic DNA, and the viral Vif protein counteracted its activity. Thus, APOBEC family members might have evolved as a general defense mechanism of the body against retroviruses, retrotransposons, and other mobile genetic elements.
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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.