ArticleJournal of acquired immune deficiency syndromes (1999)2014
Discordance between peripheral and colonic markers of inflammation during suppressive ART.
Article in Journal of acquired immune deficiency syndromes (1999), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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
24 citing papers in PubMed, 31 citations in OpenAlex.
- Randomized Trial of Ruxolitinib in Antiretroviral-Treated Adults With Human Immunodeficiency Virus.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022Trial
- Targeting the pDC/IFN-I axis in HIV-1 immunotherapy.Current opinion in HIV and AIDS · 2026Review
- Persistent Type I Interferon Signaling Impairs Innate Lymphoid Cells During HIV-1 Infection Under Suppressive ART.Viruses · 2025Article
- Increased IFN responses drive myeloid cell activation in people living with HIV-1.Scientific reports · 2025Article
- P-selectin glycoprotein ligand-1 and cardiovascular diseases: from a general perspective to an HIV infection context.Frontiers in cardiovascular medicine · 2025Article
- Identification of the shared hub gene signatures and molecular mechanisms between HIV-1 and pulmonary arterial hypertension.Scientific reports · 2024Article
- PSGL-1, a Strategic Biomarker for Pathological Conditions in HIV Infection: A Hypothesis Review.Viruses · 2023Review
- Cellular and molecular insights into incomplete immune recovery in HIV/AIDS patients.Frontiers in immunology · 2023Review
- Type I interferons and TGF-β cooperate to induce liver fibrosis during HIV-1 infection under antiretroviral therapy.JCI insight · 2022Article
- Alterations in circulating markers in HIV/AIDS patients with poor immune reconstitution: Novel insights from microbial translocation and innate immunity.Frontiers in immunology · 2022Review
- Antigen Presenting Cells Contribute to Persistent Immune Activation Despite Antiretroviral Therapy Initiation During Hyperacute HIV-1 Infection.Frontiers in immunology · 2021Article
- Activation and gut-homing of peripheral T cells in HIV immunologic non-responders despite long term viral suppression.PloS one · 2021Article
- Review
- Pathogenic Role of Type I Interferons in HIV-Induced Immune Impairments in Humanized Mice.Current HIV/AIDS reports · 2019Review
- Manipulating the Interferon Signaling Pathway: Implications for HIV Infection.Virologica Sinica · 2019Review
- Type I IFN signaling blockade by a PASylated antagonist during chronic SIV infection suppresses specific inflammatory pathways but does not alter T cell activation or virus replication.PLoS pathogens · 2018Article
- HBV and HIV viral load but not microbial translocation or immune activation are associated with liver fibrosis among patients in South Africa.BMC infectious diseases · 2018Article
- Type I interferons suppress viral replication but contribute to T cell depletion and dysfunction during chronic HIV-1 infection.JCI insight · 2017Article
- Blocking type I interferon signaling enhances T cell recovery and reduces HIV-1 reservoirs.The Journal of clinical investigation · 2017Article
- The interferon paradox: can inhibiting an antiviral mechanism advance an HIV cure?The Journal of clinical investigation · 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 4 institutions in 1 country.
Funding
Abstract
objectivePersistent systemic inflammation is associated with the inability of some HIV-infected patients to normalize circulating CD4 T-cell levels after years of suppressive antiretroviral therapy. In this study, we sought to understand whether such systemic inflammation is also associated with detectable signs of inflammation in biopsies from the rectosigmoid colon.
designImmunologic and virological parameters were studied in the peripheral blood and in rectosigmoid colon biopsies from individuals with viral suppression for at least 2 years and with peripheral CD4 T-cell levels of <350 cells per cubic millimeter (immunologic nonresponders, n = 18) or >500 cells per cubic millimeter (immunologic responders, n = 16).
methodsPeripheral blood and rectosigmoid colon biopsies were analyzed by flow cytometry, enzyme-linked immunosorbent assay, and quantitative polymerase chain reaction.
resultsNonresponders had elevated T-cell activation and inflammatory cytokines in the circulation, but inflammatory gene expression in colon biopsies was not different as compared with responders, and there was little relationship between blood and colon markers of inflammation. Blood inflammatory markers were positively associated with soluble CD14 levels indicative of monocyte activation.
conclusionsThese findings demonstrate that, in the context of treated HIV disease, it is easier to detect parameters of inflammation (including blood monocyte activation) in the peripheral blood than in isolated rectosigmoid colon biopsies. Accordingly, interventions to block such inflammation in this population might be most conveniently and accurately assessed in blood.
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.