ArticleJournal of virology2012
APOBEC3A, APOBEC3B, and APOBEC3H haplotype 2 restrict human T-lymphotropic virus type 1.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed, 96 citations in OpenAlex.
- Lack of association between intact/deletion polymorphisms of the APOBEC3B gene and HIV-1 risk.PloS one · 2014Trial
- Mechanisms of APOBEC3 Packaging into HIV-1.Viruses · 2026Review
- Article
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- Properties and Mechanisms of Deletions, Insertions, and Substitutions in the Evolutionary History of SARS-CoV-2.International journal of molecular sciences · 2024Review
- Viral infection, APOBEC3 dysregulation, and cancer.Frontiers in genetics · 2024Review
- Developing a highly efficient CGBE base editor in watermelon.Horticulture research · 2023Article
- Article
- Mechanisms of Innate Immune Sensing of HTLV-1 and Viral Immune Evasion.Pathogens (Basel, Switzerland) · 2023Review
- APOBEC3B drives PKR-mediated translation shutdown and protects stress granules in response to viral infection.Nature communications · 2023Article
- The APOBEC3B cytidine deaminase is an adenovirus restriction factor.PLoS pathogens · 2023Article
- APOBEC3: Friend or Foe in Human Papillomavirus Infection and Oncogenesis?Annual review of virology · 2022Review
- Review
- APOBEC3A regulates transcription from interferon-stimulated response elements.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Molecular Biology and Diversification of Human Retroviruses.Frontiers in virology (Lausanne, Switzerland) · 2022Article
- New Insights Into the Lineage-Specific Expansion and Functional Diversification of Lamprey AID/APOBEC Family.Frontiers in immunology · 2022Article
- Interaction with the CCT chaperonin complex limits APOBEC3A cytidine deaminase cytotoxicity.EMBO reports · 2021Article
- Transcriptomic profiling and genomic mutational analysis of Human coronavirus (HCoV)-229E -infected human cells.PloS one · 2021Article
- Deaminase-Independent Mode of Antiretroviral Action in Human and Mouse APOBEC3 Proteins.Microorganisms · 2020Review
- The Role of APOBECs in Viral Replication.Microorganisms · 2020Review
13 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
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The human APOBEC3 family consists of seven cytidine deaminases (A3A to A3H), some of which display potent antiretroviral activity against HIV-1 and other retroviruses. Studies that analyzed the effect of A3G on human T-lymphotropic virus type 1 (HTLV-1) infectivity resulted in conflicting findings, and our knowledge of HTLV-1 restriction by other A3 proteins remains limited. Since HTLV-1, much like HIV, targets CD4(+) T cells, we hypothesized that A3 proteins other than A3G restrict HTLV-1. All seven human A3 proteins were tested in HTLV-1 reporter and HIV-1 infectivity assays. We show that A3A, A3B, and A3H haplotype 2 (A3H hapII) acted as potent inhibitors of HTLV-1. Wild-type HIV-1, in contrast, was restricted by A3B and A3H hapII, but not by A3A. Catalytic site mutants of A3A, A3B, and A3H hapII showed that A3A and A3B restriction of HTLV-1 required deaminase activity. However, A3H hapII acted in a deaminase-independent manner when restricting HTLV-1, while requiring deaminase activity for HIV-1 restriction. We also analyzed A3 editing of HTLV-1 in five T-cell lines obtained from HTLV-1-infected patients. These cell lines contained extensively edited HTLV-1 sequences with G-to-A mutations in dinucleotide contexts suggestive of APOBEC3 mutagenesis. Comparison of the A3-induced mutations from reporter cells and the patient-derived cell lines indicate that A3G but also other A3 members, possibly A3A and A3B, affect HTLV-1 in vivo. Taken together, our data indicate that HTLV-1 is a likely target for multiple A3 proteins.
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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.