ArticleAIDS (London, England)2009
Delayed loss of control of plasma lipopolysaccharide levels after therapy interruption in chronically HIV-1-infected patients.
Article in AIDS (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses 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
34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 47 citations in OpenAlex.
- Pooled it
- The role of lipopolysaccharide as a marker of immune activation in HIV-1 infected patients: a systematic literature review.Virology journal · 2012Pooled it
- Pre-Digested Protein Enteral Nutritional Supplementation Enhances Recovery of CD4Frontiers in immunology · 2021Trial
- Trial
- Increased microbial translocation in ≤ 180 days old perinatally human immunodeficiency virus-positive infants as compared with human immunodeficiency virus-exposed uninfected infants of similar age.The Pediatric infectious disease journal · 2011Trial
- Circulating Biomarker Panorama in HIV-Associated Lymphoma: A Bridge from Early Risk Warning to Prognostic Stratification.Biomolecules · 2025Review
- Coordinated Induction of Antimicrobial Response Factors in Systemic Lupus Erythematosus.Frontiers in immunology · 2019Article
- The proportion of different interleukin-17-producing T-cell subsets is associated with liver fibrosis in chronic hepatitis C.Immunology · 2017Article
- Gut epithelial barrier dysfunction in human immunodeficiency virus-hepatitis C virus coinfected patients: Influence on innate and acquired immunity.World journal of gastroenterology · 2016Review
- Risk of coronary heart disease in patients with HIV infection.Nature reviews. Cardiology · 2014Review
- Intestinal barrier dysfunction in HIV infection: pathophysiology, clinical implications and potential therapies.Infection · 2014Review
- Immune activation is associated with increased gut microbial translocation in treatment-naive, HIV-infected children in a resource-limited setting.Journal of acquired immune deficiency syndromes (1999) · 2014Article
- Article
- Microbial translocation and liver disease progression in women coinfected with HIV and hepatitis C virus.The Journal of infectious diseases · 2013Article
- Relevance of lipopolysaccharide levels in HIV-associated neurocognitive impairment: the Neuradapt study.Journal of neurovirology · 2013Article
- Microbial translocation in the pathogenesis of HIV infection and AIDS.Clinical microbiology reviews · 2013Review
- Microbial translocation, immune activation, and HIV disease.Trends in microbiology · 2013Review
- HIV-specific immune dysregulation and atherosclerosis.Current HIV/AIDS reports · 2012Review
- Microbial translocation in HIV infection: causes, consequences and treatment opportunities.Nature reviews. Microbiology · 2012Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveIncreased circulating levels of lipopolysaccharide (LPS) have been demonstrated in HIV-1-infected progressors. We investigated the effect of antiretroviral therapy (ART) interruptions on plasma LPS levels. DESIGN AND
methodsOverall, 77 individuals participated in this study (51 HIV-positive and 26 healthy). Ten out of 51 HIV-positive participants were viremic ART-naive patients and 41 out of 51 were chronically suppressed patients on ART (three or more drugs, CD4 cell count more than 400 cells/microl, HIV-1 RNA less than 500 copies/ml for more than 8 months, less than 50 copies/ml at recruitment) undergoing therapy interruption. The limulus amebocyte assay was used to measure plasma LPS levels; enzyme-linked immunosorbent assay to measure plasma levels of endotoxin-core antibodies (EndoCAb), soluble (s)CD14, LPS-binding protein and IFN-alpha; immunoblotting to measure plasma gelsolin levels; and same day whole blood flow cytometry to measure levels of T-cell-activation markers (CD8/CD38, CD8/HLA-DR and CD3/CD95).
resultsIncreases in viremia and T-cell-activation markers were observed during therapy interruptions. During short-term therapy interruptions of less than 12 weeks, no change in LPS levels was found, whereas negative associations between viral load and LPS levels (Spearman's Rho = -0.612, P = 0.0152), viral load and EndoCAb change (DeltaEndoCAb, correlation = -0.502, P = 0.0204), and between DeltaLPS and DeltaEndoCAb (correlation = -0.851, P = 0.0073) were observed. In contrast, increased LPS (P = 0.0171) and sCD14 (P < 0.0001) levels were observed during long-term therapy interruption of more than 12 weeks compared with levels during ART, together with no association between LPS and viral load or EndoCAb. No association between immune activation and LPS was evident at any time point.
conclusionIncreased plasma LPS levels were observed only after more than 12 weeks of ART interruption, despite presence of LPS-controlling host mechanisms.
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.