ArticleAIDS (London, England)2015
Low SAMHD1 expression following T-cell activation and proliferation renders CD4+ T cells susceptible to HIV-1.
Article in AIDS (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 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
- The Activation State of CD4 T Cells Alters Cellular Peptidase Activities, HIV Antigen Processing, and MHC Class I Presentation in a Sequence-Dependent Manner.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- In vivo CAR T cell generation using retargeted and functionalized lentiviral vectors with reduced immunogenicity.Nature communications · 2026Article
- Identification of inducible HIV reservoirs in tonsillar, intestinal and cervical tissue models of HIV latency.Nature communications · 2025Article
- Vitamin D Decreases Susceptibility of CD4Biomolecules · 2025Article
- Antigen specificities of HIV-infected cells: A role in infection and persistence?Journal of virus eradication · 2023Review
- Th17 CD4+ T-Cell as a Preferential Target for HIV Reservoirs.Frontiers in immunology · 2022Review
- SAMHD1 expression is associated with low immune activation but not correlated with HIV‑1 DNA levels in CD4+ T cells of patients with HIV‑1.Molecular medicine reports · 2020Article
- Despite early antiretroviral therapy effector memory and follicular helper CD4 T cells are major reservoirs in visceral lymphoid tissues of SIV-infected macaques.Mucosal immunology · 2020Article
- Increased SAMHD1 transcript expression correlates with interferon-related genes in HIV-1-infected patients.Medical microbiology and immunology · 2019Article
- Proliferative memory SAMHD1low CD4+ T cells harbour high levels of HIV-1 with compartmentalized viral populations.PLoS pathogens · 2019Article
- BCL6 Inhibitor-Mediated Downregulation of Phosphorylated SAMHD1 and T Cell Activation Are Associated with Decreased HIV Infection and Reactivation.Journal of virology · 2019Article
- Peering into the HIV reservoir.Reviews in medical virology · 2018Review
- Differential Effects of Strategies to Improve the Transduction Efficiency of Lentiviral Vector that Conveys an Anti-HIV Protein, Nullbasic, in Human T Cells.Virologica Sinica · 2018Article
- T Cell Subsets in the Germinal Center: Lessons from the Macaque Model.Frontiers in immunology · 2018Review
- HIV-1 Infection of Primary CD4Journal of virology · 2018Article
- Follicular CD4 T Helper Cells As a Major HIV Reservoir Compartment: A Molecular Perspective.Frontiers in immunology · 2018Review
- CD81 association with SAMHD1 enhances HIV-1 reverse transcription by increasing dNTP levels.Nature microbiology · 2017Article
- Brain Microglial Cells Are Highly Susceptible to HIV-1 Infection and Spread.AIDS research and human retroviruses · 2017Article
- HIV-1 selectively targets gut-homing CCR6+CD4+ T cells via mTOR-dependent mechanisms.JCI insight · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesHIV-1 replication depends on the state of cell activation and division. It is established that SAMHD1 restricts HIV-1 infection of resting CD4 T cells. The modulation of SAMHD1 expression during T-cell activation and proliferation, however, remains unclear, as well as a role for SAMHD1 during HIV-1 pathogenesis.
methodsSAMHD1 expression was assessed in CD4 T cells after their activation and in-vitro HIV-1 infection. We performed phenotype analyzes using flow cytometry on CD4 T cells from peripheral blood and lymph nodes from cohorts of HIV-1-infected individuals under antiretroviral treatment or not, and controls.
resultsWe show that SAMHD1 expression decreased during CD4 T-cell proliferation in association with an increased susceptibility to in-vitro HIV-1 infection. Additionally, circulating memory CD4 T cells are enriched in cells with low levels of SAMHD1. These SAMHD1 cells are highly differentiated, exhibit a large proportion of Ki67 cycling cells and are enriched in T-helper 17 cells. Importantly, memory SAMHD1 cells were depleted from peripheral blood of HIV-infected individuals. We also found that follicular helper T cells present in secondary lymphoid organs lacked the expression of SAMHD1, which was accompanied by a higher susceptibility to HIV-1 infection in vitro.
conclusionWe demonstrate that SAMHD1 expression is decreased during CD4 T-cell activation and proliferation. Also, CD4 T-cell subsets known to be more susceptible to HIV-1 infection, for example, T-helper 17 and follicular helper T cells, display lower levels of SAMHD1. These results pin point a role for SAMHD1 expression in HIV-1 infection and the concomitant depletion of CD4 T cells.
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.