ArticleJournal of virology2013
Endothelial cell stimulation overcomes restriction and promotes productive and latent HIV-1 infection of resting CD4+ T cells.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 28 citations in OpenAlex.
- The loss of glycoprotein nonmetastatic melanoma protein B (GPNMB) alters endothelial cell permeability, metabolism, and survival during infectious challenge.Clinical science (London, England : 1979) · 2026Article
- Intestinal endothelial cells increase HIV infection and latency in resting and activated CD4 + T cells, particularly affecting CCR6 + CD4 + T cells.Retrovirology · 2023Article
- HIV rapidly targets a diverse pool of CD4Immunity · 2023Article
- Endothelial Cells Promote Productive HIV Infection of Resting CD4AIDS research and human retroviruses · 2022Article
- Article
- IFNγ, and to a Lesser Extent TNFα, Provokes a Sustained Endothelial Costimulatory Phenotype.Frontiers in immunology · 2021Article
- HIV Reactivation in Latently Infected Cells With Virological Synapse-Like Cell Contact.Viruses · 2020Article
- Mechanisms of HIV-1 cell-to-cell transmission and the establishment of the latent reservoir.Virus research · 2019Review
- Lymphatic endothelial cells promote productive and latent HIV infection in resting CD4+ T cells.Virology journal · 2018Article
- CD4AIDS research and human retroviruses · 2018Review
- Review
- Mucosal stromal fibroblasts markedly enhance HIV infection of CD4+ T cells.PLoS pathogens · 2017Article
- Soluble Factors Secreted by Endothelial Cells Allow for Productive and Latent HIV-1 Infection in Resting CD4AIDS research and human retroviruses · 2017Article
- HIV integration and the establishment of latency in CCL19-treated resting CD4(+) T cells require activation of NF-κB.Retrovirology · 2016Article
- HIV-1 latency and virus production from unintegrated genomes following direct infection of resting CD4 T cells.Retrovirology · 2016Article
- Understanding Factors That Modulate the Establishment of HIV Latency in Resting CD4+ T-Cells In Vitro.PloS one · 2016Article
- The role of antigen presenting cells in the induction of HIV-1 latency in resting CD4(+) T-cells.Retrovirology · 2015Article
- HIV Latency Is Established Directly and Early in Both Resting and Activated Primary CD4 T Cells.PLoS pathogens · 2015Article
- Human immunodeficiency virus (HIV)-1 integration sites in viral latency.Current HIV/AIDS reports · 2015Review
- Targeting HIV latency: resting memory T cells, hematopoietic progenitor cells and future directions.Expert review of anti-infective therapy · 2014Review
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 3 institutions in 1 country.
Funding
Abstract
Highly active antiretroviral therapy (HAART) is able to suppress human immunodeficiency virus type 1 (HIV-1) to undetectable levels in the majority of patients, but eradication has not been achieved because latent viral reservoirs persist, particularly in resting CD4(+) T lymphocytes. It is generally understood that HIV-1 does not efficiently infect resting CD4(+) T cells, and latent infection in those cells may arise when infected CD4(+) T lymphoblasts return to resting state. In this study, we found that stimulation by endothelial cells can render resting CD4(+) T cells permissible for direct HIV infection, including both productive and latent infection. These stimulated T cells remain largely phenotypically unactivated and show a lower death rate than activated T cells, which promotes the survival of infected cells. The stimulation by endothelial cells does not involve interleukin 7 (IL-7), IL-15, CCL19, or CCL21. Endothelial cells line the lymphatic vessels in the lymphoid tissues and have frequent interactions with T cells in vivo. Our study proposes a new mechanism for infection of resting CD4(+) T cells in vivo and a new mechanism for latent infection in resting CD4(+) T cells.
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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.