ReviewFrontiers in microbiology2020
Dual Functionality of HIV-1 Vif in APOBEC3 Counteraction and Cell Cycle Arrest.
Review in Frontiers in microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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
21 citing papers in PubMed.
- Review
- 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
- Identification of Epstein-Barr virus BORF2 sequences required for APOBEC3B relocalization.Journal of virology · 2025Article
- MicroRNAs in HIV infection: dual regulators of viral replication and host immunity.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Role of HIV-encoded proteins in cardiovascular disease.American journal of physiology. Cell physiology · 2025Review
- Article
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- HIV-1 Vif protein sequence variations in South African people living with HIV and their influence on Vif-APOBEC3G interaction.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2024Article
- Review
- Inhibition of ATM-directed antiviral responses by HIV-1 Vif.PLoS pathogens · 2023Article
- Article
- HIV-1 virological synapse formation enhances infection spread by dysregulating Aurora Kinase B.PLoS pathogens · 2023Article
- 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
- Evolutionary Conservation of PP2A Antagonism and G2/M Cell Cycle Arrest in Maedi-Visna Virus Vif.Viruses · 2022Article
- Defective HIV-1 genomes and their potential impact on HIV pathogenesis.Retrovirology · 2022Review
- Global post-translational modification profiling of HIV-1-infected cells reveals mechanisms of host cellular pathway remodeling.Cell reports · 2022Article
- HIV-1 Accessory Proteins Impart a Modest Interferon Response and Upregulate Cell Cycle-Related Genes in Macrophages.Pathogens (Basel, Switzerland) · 2022Article
- Special Issue "APOBECs and Virus Restriction".Viruses · 2021Article
- Human APOBEC3 Variations and Viral Infection.Viruses · 2021Review
- Potential Utilization of APOBEC3-Mediated Mutagenesis for an HIV-1 Functional Cure.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Accessory proteins are a key feature that distinguishes primate immunodeficiency viruses such as human immunodeficiency virus type I (HIV-1) from other retroviruses. A prime example is the virion infectivity factor, Vif, which hijacks a cellular co-transcription factor (CBF-β) to recruit a ubiquitin ligase complex (CRL5) to bind and degrade antiviral APOBEC3 enzymes including APOBEC3D (A3D), APOBEC3F (A3F), APOBEC3G (A3G), and APOBEC3H (A3H). Although APOBEC3 antagonism is essential for viral pathogenesis, and a more than sufficient functional justification for Vif's evolution, most viral proteins have evolved multiple functions. Indeed, Vif has long been known to trigger cell cycle arrest and recent studies have shed light on the underlying molecular mechanism. Vif accomplishes this function using the same CBF-β/CRL5 ubiquitin ligase complex to degrade a family of PPP2R5 phospho-regulatory proteins. These advances have helped usher in a new era of accessory protein research and fresh opportunities for drug development.
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Registered trials
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