ArticleJournal of virology2010
APOBEC3G generates nonsense mutations in human T-cell leukemia virus type 1 proviral genomes in vivo.
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 80 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.
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Who cites it
80 citing papers in PubMed, 121 citations in OpenAlex.
- Immunophenotype and proviral landscape of HTLV-1c infection and pulmonary disease.EBioMedicine · 2026Article
- Viral-driven oncogenesis in T/NK-cell lymphomas: parallels and divergences between HTLV-1 and EBV.International journal of hematology · 2026Review
- Review
- Long-term kinetics of proviral load in HTLV-1 carriers: defining risk for the development of adult T-cell leukemia/lymphoma.Biomarker research · 2025Article
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- Article
- Highly homologous simian T-cell leukemia virus type 1 genome in Japanese macaques: a large cohort study.Virology journal · 2024Article
- Vulnerability to APOBEC3G linked to the pathogenicity of deltaretroviruses.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Establishment of a novel human T-cell leukemia virus type 1 infection model using cell-free virus.Journal of virology · 2024Article
- Geographic characteristics of HTLV-1 molecular subgroups and genetic substitutions in East Asia: Insights from complete genome sequencing of HTLV-1 strains isolated in Taiwan and Japan.PLoS neglected tropical diseases · 2024Article
- The transcriptome of HTLV-1-infected primary cells following reactivation reveals changes to host gene expression central to the proviral life cycle.PLoS pathogens · 2023Article
- Viral, genetic, and immune factors in the oncogenesis of adult T-cell leukemia/lymphoma.International journal of hematology · 2023Review
- Geographic distribution, clinical epidemiology and genetic diversity of the human oncogenic retrovirus HTLV-1 in Africa, the world's largest endemic area.Frontiers in immunology · 2023Review
- Review
- Article
- Review
- HTLV-1 persistence and leukemogenesis: A game of hide-and-seek with the host immune system.Frontiers in immunology · 2022Review
- Alternative RNA splicing in cancer: what about adult T-cell leukemia?Frontiers in immunology · 2022Review
- Loss of function mutations inAmerican journal of cancer research · 2022Article
- The HTLV-1 proviral status is a potential prognostic biomarker for adult T-cell leukemia-lymphoma treated with allogeneic stem cell transplantation.Bone marrow transplantation · 2021Article
20 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
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human T-cell leukemia virus type 1 (HTLV-1) induces cell proliferation after infection, leading to efficient transmission by cell-to-cell contact. After a long latent period, a fraction of carriers develop adult T-cell leukemia (ATL). Genetic changes in the tax gene in ATL cells were reported in about 10% of ATL cases. To determine genetic changes that may occur throughout the provirus, we determined the entire sequence of the HTLV-1 provirus in 60 ATL cases. Abortive genetic changes, including deletions, insertions, and nonsense mutations, were frequent in all viral genes except the HBZ gene, which is transcribed from the minus strand of the virus. G-to-A base substitutions were the most frequent mutations in ATL cells. The sequence context of G-to-A mutations was in accordance with the preferred target sequence of human APOBEC3G (hA3G). The target sequences of hA3G were less frequent in the plus strand of the HBZ coding region than in other coding regions of the HTLV-1 provirus. Nonsense mutations in viral genes including tax were also observed in proviruses from asymptomatic carriers, indicating that these mutations were generated during reverse transcription and prior to oncogenesis. The fact that hA3G targets the minus strand during reverse transcription explains why the HBZ gene is not susceptible to such nonsense mutations. HTLV-1-infected cells likely take advantage of hA3G to escape from the host immune system by losing expression of viral 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.