ReviewRetrovirology2013
HIV restriction in quiescent CD4⁺ T cells.
Review in Retrovirology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Identification of novel HIV-1 dependency factors in primary CCR4(+)CCR6(+)Th17 cells via a genome-wide transcriptional approach.Retrovirology · 2015Pooled it
- Healthy dynamics of CD4 T cells may drive HIV resurgence in perinatally-infected infants on antiretroviral therapy.PLoS pathogens · 2022Article
- Exacerbated AIDS Progression by PD-1 Blockade during Therapeutic Vaccination in Chronically Simian Immunodeficiency Virus-Infected Rhesus Macaques after Interruption of Antiretroviral Therapy.Journal of virology · 2022Article
- Endothelial Cells Promote Productive HIV Infection of Resting CD4AIDS research and human retroviruses · 2022Article
- Review
- Hsa-miR-31 Governs T-Cell Homeostasis in HIV ProtectionFrontiers in immunology · 2021Article
- Phyloanatomic characterization of the distinct T cell and monocyte contributions to the peripheral blood HIV population within the host.Virus evolution · 2020Article
- CD4 T Cell Metabolism Is a Major Contributor of HIV Infectivity and Reservoir Persistence.Immunometabolism · 2020Article
- Spatially clustered loci with multiple enhancers are frequent targets of HIV-1 integration.Nature communications · 2019Article
- CD4Physiological reports · 2019Article
- Entry of glucose- and glutamine-derived carbons into the citric acid cycle supports early steps of HIV-1 infection in CD4 T cells.Nature metabolism · 2019Article
- The role of integration and clonal expansion in HIV infection: live long and prosper.Retrovirology · 2018Review
- IL-15 regulates susceptibility of CD4Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Myeloid Dendritic Cells Induce HIV Latency in Proliferating CD4Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Incomplete Suppression of HIV-1 by SAMHD1 Permits Efficient Macrophage Infection.Pathogens & immunity · 2018Article
- Single-cell analysis identifies cellular markers of the HIV permissive cell.PLoS pathogens · 2017Article
- HIV-1 Vpr- and Reverse Transcription-Induced Apoptosis in Resting Peripheral Blood CD4 T Cells and Protection by Common Gamma-Chain Cytokines.Journal of virology · 2016Article
- Understanding Factors That Modulate the Establishment of HIV Latency in Resting CD4+ T-Cells In Vitro.PloS one · 2016Article
- COMMD1/Murr1 reinforces HIV-1 latent infection through IκB-α stabilization.Journal of virology · 2015Article
- Bioinformatics and HIV latency.Current HIV/AIDS reports · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The restriction of the Human Immunodeficiency Virus (HIV) infection in quiescent CD4⁺ T cells has been an area of active investigation. Early studies have suggested that this T cell subset is refractory to infection by the virus. Subsequently it was demonstrated that quiescent cells could be infected at low levels; nevertheless these observations supported the earlier assertions of debilitating defects in the viral life cycle. This phenomenon raised hopes that identification of the block in quiescent cells could lead to the development of new therapies against HIV. As limiting levels of raw cellular factors such as nucleotides did not account for the block to infection, a number of groups pursued the identification of cellular proteins whose presence or absence may impact the permissiveness of quiescent T cells to HIV infection. A series of studies in the past few years have identified a number of host factors implicated in the block to infection. In this review, we will present the progress made, other avenues of investigation and the potential impact these studies have in the development of more effective therapies against HIV.
Indexed as
Identifiers
What OpenQuestion holds
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.