ArticleJournal of virology1998
Naïve and memory CD4 T cells differ in their susceptibilities to human immunodeficiency virus type 1 infection following CD28 costimulation: implicatip6s for transmission and pathogenesis.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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Who cites it
27 citing papers in PubMed, 72 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
- Exercise to Prevent Accelerated Vascular Aging in People Living With HIV.Circulation research · 2024Review
- Transforming Growth Factor β Signaling Promotes HIV-1 Infection in Activated and Resting Memory CD4Journal of virology · 2023Article
- The Effect of Treatment-Associated Mutations on HIV Replication and Transmission Cycles.Viruses · 2022Review
- Heterogeneity of Latency Establishment in the Different Human CD4Journal of virology · 2022Article
- Challenges and Opportunities of Using Adoptive T-Cell Therapy as Part of an HIV Cure Strategy.The Journal of infectious diseases · 2021Review
- Methamphetamine functions as a novel CD4Scientific reports · 2019Article
- HIV Infected T Cells Can ProliferateFrontiers in microbiology · 2019Article
- Article
- RNAi-Mediated CCR5 Knockdown Provides HIV-1 Resistance to Memory T Cells in Humanized BLT Mice.Molecular therapy. Nucleic acids · 2015Article
- Defining the fitness of HIV-1 isolates with dual/mixed co-receptor usage.AIDS research and therapy · 2015Article
- Genome-wide search for the genes accountable for the induced resistance to HIV-1 infection in activated CD4+ T cells: apparent transcriptional signatures, co-expression networks and possible cellular processes.BMC medical genomics · 2013Article
- HIV-1 Nef and T-cell activation: a history of contradictions.Future virology · 2013Article
- Kruppel-like factor 2 modulates CCR5 expression and susceptibility to HIV-1 infection.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Asymmetric HIV-1 co-receptor use and replication in CD4(+) T lymphocytes.Journal of translational medicine · 2011Review
- Effective activation alleviates the replication block of CCR5-tropic HIV-1 in chimpanzee CD4+ lymphocytes.Virology · 2009Article
- Human immunodeficiency virus integrates directly into naive resting CD4+ T cells but enters naive cells less efficiently than memory cells.Journal of virology · 2009Article
- Self-protection of individual CD4+ T cells against R5 HIV-1 infection by the synthesis of anti-viral CCR5 ligands.PloS one · 2008Article
- Differential susceptibility of naïve, central memory and effector memory T cells to dendritic cell-mediated HIV-1 transmission.Retrovirology · 2006Article
- Lewis X component in human milk binds DC-SIGN and inhibits HIV-1 transfer to CD4+ T lymphocytes.The Journal of clinical investigation · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In vitro evidence suggests that memory CD4(+) cells are preferentially infected by human immunodeficiency virus type 1 (HIV-1), yet studies of HIV-1-infected individuals have failed to detect preferential memory cell depletion. To explore this paradox, we stimulated CD45RA+ CD4(+) (naïve) and CD45RO+ CD4(+) (memory) cells with antibodies to CD3 and CD28 and infected them with either CCR5-dependent (R5) or CXCR4-dependent (X4) HIV-1 isolates. Naïve CD4(+) cells supported less X4 HIV replication than their memory counterparts. However, naïve cells were susceptible to R5 viral infection, while memory cells remained resistant to infection and viral replication. As with the unseparated cells, mixing the naïve and memory cells prior to infection resulted in cells resistant to R5 infection and highly susceptible to X4 infection. While both naïve and memory CD4(+) subsets downregulated CCR5 expression in response to CD28 costimulation, only the memory cells produced high levels of the beta-chemokines RANTES, MIP-1alpha, and MIP-1beta upon stimulation. Neutralization of these beta-chemokines rendered memory CD4(+) cells highly sensitive to infection with R5 HIV-1 isolates, indicating that downregulation of CCR5 is not sufficient to mediate complete protection from CCR5 strains of HIV-1. These results indicate that susceptibility to R5 HIV-1 isolates is determined not only by the level of CCR5 expression but also by the balance of CCR5 expression and beta-chemokine production. Furthermore, our results suggest a model of HIV-1 transmission and pathogenesis in which naïve rather than memory CD4(+) T cells serve as the targets for early rounds of HIV-1 replication.
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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.