ArticlePLoS pathogens2009
Reassessing the role of APOBEC3G in human immunodeficiency virus type 1 infection of quiescent CD4+ T-cells.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Who cites it
35 citing papers in PubMed, 47 citations in OpenAlex.
- A dichotomy in cortical actin and chemotactic actin activity between human memory and naive T cells contributes to their differential susceptibility to HIV-1 infection.The Journal of biological chemistry · 2012Trial
- Efficient derivation of chimeric-antigen receptor-modified TFrontiers in immunology · 2022Article
- Increased expression with differential subcellular location of cytidine deaminase APOBEC3G in human CD4(+) T-cell activation and dendritic cell maturation.Immunology and cell biology · 2016Article
- Restrictions to HIV-1 replication in resting CD4+ T lymphocytes.Cell research · 2013Review
- Interleukin-2 inhibits HIV-1 replication in some human T cell lymphotrophic virus-1-infected cell lines via the induction and incorporation of APOBEC3G into the virion.The Journal of biological chemistry · 2013Article
- HIV restriction in quiescent CD4⁺ T cells.Retrovirology · 2013Review
- T-Cell Signaling in HIV-1 Infection.The open virology journal · 2013Article
- The role of cytidine deaminases on innate immune responses against human viral infections.BioMed research international · 2013Review
- Biochemical analysis of hypermutation by the deoxycytidine deaminase APOBEC3A.The Journal of biological chemistry · 2012Article
- Emerging complexities of APOBEC3G action on immunity and viral fitness during HIV infection and treatment.Retrovirology · 2012Review
- Multi-scale modeling of HIV infection in vitro and APOBEC3G-based anti-retroviral therapy.PLoS computational biology · 2012Article
- Engineering HIV-1-resistant T-cells from short-hairpin RNA-expressing hematopoietic stem/progenitor cells in humanized BLT mice.PloS one · 2012Article
- Endogenous origins of HIV-1 G-to-A hypermutation and restriction in the nonpermissive T cell line CEM2n.PLoS pathogens · 2012Article
- APOBEC3A is a specific inhibitor of the early phases of HIV-1 infection in myeloid cells.PLoS pathogens · 2011Article
- CD4+ T cell depletion in human immunodeficiency virus (HIV) infection: role of apoptosis.Viruses · 2011Review
- APOBEC3G: a double agent in defense.Trends in biochemical sciences · 2011Article
- R5 HIV env and vesicular stomatitis virus G protein cooperate to mediate fusion to naive CD4+ T Cells.Journal of virology · 2011Article
- Quiescent T cells and HIV: an unresolved relationship.Immunologic research · 2010Review
- Abortive HIV infection mediates CD4 T cell depletion and inflammation in human lymphoid tissue.Cell · 2010Article
- Generation of human induced pluripotent stem cells bearing an anti-HIV transgene by a lentiviral vector carrying an internal murine leukemia virus promoter.Human gene therapy · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
HIV-1 is restricted for infection of primary quiescent T-cells. After viral entry, reverse transcription is initiated but is not completed. Various hypotheses have been proposed for this cellular restriction including insufficient nucleotide pools and cellular factors, but none have been confirmed as the primary mechanism for restriction. A recent study by Chiu et al. implicates APOBEC3G, an anti-retroviral cytidine deaminase, as the cellular restriction factor. Here, we attempted to confirm these findings using the same strategy as reported by Chiu et al. of siRNA targeting knock-down of APOBEC3G expression. In contrast to the published study, our results do not support a role for APOBEC3G in restriction of HIV-1 in quiescent CD4+ T-cells. In our study, we tested the same siRNA as reported by Chiu et al. as well as two additional siRNAs targeting APOBEC3G, one of which showed 2-fold greater knock-down of APOBEC3G mRNA. However, none of the three siRNAs tested had a discernable effect on enhancing infection by HIV-1 in quiescent CD4+ T-cells. Therefore, we conclude that the primary mechanism of HIV-1 restriction in quiescent CD4+ T-cells remains to be elucidated.
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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.