ArticleThe Journal of experimental medicine2010
The antiviral factor APOBEC3G improves CTL recognition of cultured HIV-infected T cells.
Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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Who cites it
55 citing papers in PubMed, 86 citations in OpenAlex.
- Longitudinal study reveals HIV-1-infected CD4+ T cell dynamics during long-term antiretroviral therapy.The Journal of clinical investigation · 2020Trial
- HIV proviral transcription and infectivity are enhanced by neddylation.Journal of virology · 2025Article
- Non-AUG HIV-1 uORF translation elicits specific T cell immune response and regulates viral transcript expression.Nature communications · 2025Article
- APOBEC3-Related Editing and Non-Editing Determinants of HIV-1 and HTLV-1 Restriction.International journal of molecular sciences · 2025Review
- Intact HIV Proviruses Persist in the Brain Despite Viral Suppression with ART.Annals of neurology · 2022Article
- Examination of the APOBEC3 Barrier to Cross Species Transmission of Primate Lentiviruses.Viruses · 2021Review
- Human TRIM5α: Autophagy Connects Cell-Intrinsic HIV-1 Restriction and Innate Immune Sensor Functioning.Viruses · 2021Review
- Potential Utilization of APOBEC3-Mediated Mutagenesis for an HIV-1 Functional Cure.Frontiers in microbiology · 2021Review
- The interesting relationship between APOBEC3 deoxycytidine deaminases and cancer: a long road ahead.Open biology · 2020Article
- Article
- Variable gene expression and parasite load predict treatment outcome in cutaneous leishmaniasis.Science translational medicine · 2019Article
- Review
- Article
- Co- but not Sequential Infection of DCs Boosts Their HIV-Specific CTL-Stimulatory Capacity.Frontiers in immunology · 2019Article
- Restriction Factors: From Intrinsic Viral Restriction to Shaping Cellular Immunity Against HIV-1.Frontiers in immunology · 2018Review
- APOBEC3G Regulation of the Evolutionary Race Between Adaptive Immunity and Viral Immune Escape Is Deeply Imprinted in the HIV Genome.Frontiers in immunology · 2018Article
- Host Restriction Factors APOBEC3G/3F and Other Interferon-Related Gene Expressions Affect Early HIV-1 Infection in Northern Pig-Tailed Macaque (Frontiers in immunology · 2018Article
- Evasion of adaptive immunity by HIV through the action of host APOBEC3G/F enzymes.AIDS research and therapy · 2017Review
- The role of MHC class I gene products in SIV infection of macaques.Immunogenetics · 2017Review
- Mechanisms of HIV-1 Control.Current HIV/AIDS reports · 2017Review
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
The cytidine deaminase APOBEC3G (A3G) enzyme exerts an intrinsic anti-human immunodeficiency virus (HIV) defense by introducing lethal G-to-A hypermutations in the viral genome. The HIV-1 viral infectivity factor (Vif) protein triggers degradation of A3G and counteracts this antiviral effect. The impact of A3G on the adaptive cellular immune response has not been characterized. We examined whether A3G-edited defective viruses, which are known to express truncated or misfolded viral proteins, activate HIV-1-specific (HS) CD8+ cytotoxic T lymphocytes (CTLs). To this end, we compared the immunogenicity of cells infected with wild-type or Vif-deleted viruses in the presence or absence of the cytidine deaminase. The inhibitory effect of A3G on HIV replication was associated with a strong activation of cocultivated HS-CTLs. CTL activation was particularly marked with Vif-deleted HIV and with viruses harboring A3G. Enzymatically inactive A3G mutants failed to enhance CTL activation. We also engineered proviruses bearing premature stop codons in their genome as scars of A3G editing. These viruses were not infectious but potently activated HS-CTLs. Therefore, the pool of defective viruses generated by A3G represents an underestimated source of viral antigens. Our results reveal a novel function for A3G, acting not only as an intrinsic antiviral factor but also as an inducer of the adaptive immune system.
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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.