ArticleBlood2013
Distinct gene-expression profiles associated with the susceptibility of pathogen-specific CD4 T cells to HIV-1 infection.
Article in Blood, 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, 39 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
- HCV-specific CD4EBioMedicine · 2026Article
- Chronic inflammation degrades CD4 T cell immunity to prior vaccines in treated HIV infection.Nature communications · 2024Article
- HIV Expression in Infected T Cell Clones.Viruses · 2024Review
- HSV-2 triggers upregulation of MALAT1 in CD4+ T cells and promotes HIV latency reversal.The Journal of clinical investigation · 2023Article
- Antigen specificities of HIV-infected cells: A role in infection and persistence?Journal of virus eradication · 2023Review
- Glycan dependent phenotype differences of HIV-1 generated from macrophage versus CD4Frontiers in immunology · 2023Article
- HIV persistence in subsets of CD4+ T cells: 50 shades of reservoirs.Seminars in immunology · 2021Review
- Epigenetic Suppression of HIV in Myeloid Cells by the BRD4-Selective Small Molecule Modulator ZL0580.Journal of virology · 2020Article
- The forces driving clonal expansion of the HIV-1 latent reservoir.Virology journal · 2020Review
- CD4AIDS research and human retroviruses · 2018Review
- Th17 cells differentiated with mycelial membranes of Candida albicans prevent oral candidiasis.FEMS yeast research · 2018Article
- Distinct susceptibility of HIV vaccine vector-induced CD4 T cells to HIV infection.PLoS pathogens · 2018Article
- HIV persists in CCR6+CD4+ T cells from colon and blood during antiretroviral therapy.AIDS (London, England) · 2017Article
- Sequential Dysfunction and Progressive Depletion of Candida albicans-Specific CD4 T Cell Response in HIV-1 Infection.PLoS pathogens · 2016Article
- HIV Susceptibility of human antigen-specific CD4 T cells in AIDS pathogenesis and vaccine response.Expert review of vaccines · 2016Review
- HIV Skews the Lineage-Defining Transcriptional Profile of Mycobacterium tuberculosis-Specific CD4+ T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Differences in antigen-specific CD4+ responses to opportunistic infections in HIV infection.Immunity, inflammation and disease · 2015Article
- Oropharyngeal Candidiasis in HIV Infection: Analysis of Impaired Mucosal Immune Response to Candida albicans in Mice Expressing the HIV-1 Transgene.Pathogens (Basel, Switzerland) · 2015Review
- New Insights about Treg and Th17 Cells in HIV Infection and Disease Progression.Journal of immunology research · 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
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In HIV infection, CD4 responses to opportunistic pathogens such as Candida albicans are lost early, but CMV-specific CD4 response persists. Little is currently known about HIV infection of CD4 T cells of different pathogen/antigen specificities. CFSE-labeled PBMCs were stimulated with CMV, tetanus toxoid (TT), and C albicans antigens and subsequently exposed to HIV. HIV infection was monitored by intracellular p24 in CFSE(low) population. We found that although TT- and C albicans-specific CD4 T cells were permissive, CMV-specific CD4 T cells were highly resistant to both R5 and X4 HIV. Quantification of HIV DNA in CFSE(low) cells showed a reduction of strong-stop and full-length DNA in CMV-specific cells compared with TT- and C albicans-specific cells. β-Chemokine neutralization enhanced HIV infection in TT- and C albicans-specific cells, whereas HIV infection in CMV-specific cells remained low despite increased entry by β-chemokine neutralization, suggesting postentry HIV restriction by CMV-specific cells. Microarray analysis (Gene Expression Omnibus accession number: GSE42853) revealed distinct transcriptional profiles that involved selective up-regulation of comprehensive innate antiviral genes in CMV-specific cells, whereas TT- and C albicans-specific cells mainly up-regulated Th17 inflammatory response. Our data suggest a mechanism for the persistence of CMV-specific CD4 response and earlier loss of mucosal Th17-associated TT- and C albicans-specific CD4 response in AIDS.
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.