Trial reportThe Journal of biological chemistry2012
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.
Trial report in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 36 citations in OpenAlex.
- Trial
- Discovery of actinators, actin-derived bioactive peptides that modulate cytoskeleton and actin-related cellular activities.Science advances · 2026Article
- HSV-1 infection induces brain cofilin hyperphosphorylation in the 5×FAD Alzheimer's Disease mouse model.bioRxiv : the preprint server for biology · 2025Article
- HIV Infection: Shaping the Complex, Dynamic, and Interconnected Network of the Cytoskeleton.International journal of molecular sciences · 2023Review
- 3D chromatin reprogramming primes human memory TScience immunology · 2023Article
- Cell-to-cell transmission of HIV-1 from provirus-activated cells to resting naïve and memory human primary CD4 T cells is highly efficient and requires CD4 and F-actin but not chemokine receptors.Journal of medical virology · 2022Article
- Article
- Heterogeneity of Latency Establishment in the Different Human CD4Journal of virology · 2022Article
- CounterAKTing HIV: Toward a "Block and Clear" Strategy?Frontiers in cellular and infection microbiology · 2022Review
- Prestimulation of CD2 confers resistance to HIV-1 latent infection in blood resting CD4 T cells.iScience · 2021Article
- IP-10 Promotes Latent HIV Infection in Resting Memory CD4Frontiers in immunology · 2021Article
- Establishment and Reversal of HIV-1 Latency in Naive and Central Memory CD4+ T Cells In Vitro.Journal of virology · 2016Article
- Immunophenotyping of rheumatoid arthritis reveals a linkage between HLA-DRB1 genotype, CXCR4 expression on memory CD4(+) T cells, and disease activity.Scientific reports · 2016Article
- Quantitation of replication-competent HIV-1 in populations of resting CD4+ T cells.Journal of virology · 2014Article
- Article
- HIV-1 triggers WAVE2 phosphorylation in primary CD4 T cells and macrophages, mediating Arp2/3-dependent nuclear migration.The Journal of biological chemistry · 2014Article
- Quantitative analysis of the processes and signaling events involved in early HIV-1 infection of T cells.PloS one · 2014Article
- Novel anti-HIV therapeutics targeting chemokine receptors and actin regulatory pathways.Immunological reviews · 2013Review
- Restrictions to HIV-1 replication in resting CD4+ T lymphocytes.Cell research · 2013Review
- HIV-1 transcription and latency: an update.Retrovirology · 2013Review
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 1 country.
Funding
Abstract
Human memory and naive CD4 T cells can mainly be identified by the reciprocal expression of the CD45RO or CD45RA isoforms. In HIV-1 infection, blood CD45RO memory CD4 T cells are preferentially infected and serve as a major viral reservoir. The molecular mechanism dictating this differential susceptibility to HIV-1 remains largely obscure. Here, we report that the different susceptibility of memory and naive T cells to HIV is not determined by restriction factors such as Apobec3G or BST2. However, we observed a phenotypic distinction between human CD45RO and CD45RA resting CD4 T cells in their cortical actin density and actin dynamics. CD45RO CD4 T cells possess a higher cortical actin density and can be distinguished as CD45RO(+)Actin(high). In contrast, CD45RA T cells are phenotypically CD45RA(+)Actin(low). In addition, the cortical actin in CD45RO memory CD4 T cells is more dynamic and can respond to low dosages of chemotactic induction by SDF-1, whereas that of naive cells cannot, despite a similar level of the chemokine receptor CXCR4 present on both cells. We further demonstrate that this difference in the cortical actin contributes to their differential susceptibility to HIV-1; resting memory but not naive T cells are highly responsive to HIV-mediated actin dynamics that promote higher levels of viral entry and early DNA synthesis in resting memory CD4 T cells. Furthermore, transient induction of actin dynamics in resting naive T cells rescues HIV latent infection following CD3/CD28 stimulation. These results suggest a key role of chemotactic actin activity in facilitating HIV-1 latent infection of these T cell subsets.
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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.