Evidence map›Paper›PMID 24516541›Full record

ArticlePloS one2014

HIV-1 coinfection profoundly alters intrahepatic chemokine but not inflammatory cytokine profiles in HCV-infected subjects.

Sishun Hu, Marwan Ghabril, Tohti Amet, Ningjie Hu, Daniel Byrd, Kai Yang, Raj Vuppalanchi, Romil Saxena, Mona Desai, Jie Lan and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 31% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 12 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Sishun HuDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America ; College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.
Marwan GhabrilDivision of Gastroenterology/Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Tohti AmetDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Ningjie HuZhejiang Provincial Key Laboratory for Technology & Application of Model Organisms, Wenzhou Medical College, Wenzhou, Zhejiang, China.
Daniel ByrdDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Kai YangZhejiang Provincial Key Laboratory for Technology & Application of Model Organisms, Wenzhou Medical College, Wenzhou, Zhejiang, China.
Raj VuppalanchiDivision of Gastroenterology/Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Romil SaxenaDepartment of Pathology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Mona DesaiDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America ; Division of Infectious Diseases, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Jie LanDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Raymond JohnsonDivision of Infectious Diseases, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Samir GuptaDivision of Infectious Diseases, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Naga ChalasaniDivision of Gastroenterology/Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Qigui YuDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America ; Division of Infectious Diseases, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, United States of America ; Center for AIDS Research, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Indiana University School of MedicineWenzhou Medical University · CNHuazhong Agricultural University · CNIndiana University – Purdue University Indianapolis · US

Funding

Immunology and Infectious Diseases Training ProgramT32AI060519 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MARK H KAPLAN · 2004 to 2026
$6.0M
Training in STIs and infections of global health significanceT32AI007637 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI WOOLS-KALOUSTIAN, KARA KAY · 2001 to 2020
$3.4M
EXTRAMURAL RESEARCH FACILITIES CONSTRUCTIONC06RR015481 · NCRR · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIFE, ROSE S · 2001 to 2001
$1.6M
Specific killing of latently HIV-1-infected cells after provirus reactivationR21AI104268 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI YU, QIGUI A. · 2013 to 2014
$429k
NCRR NIH HHS C06 RR015481NCRR NIH HHS C06 RR015481-01NIAID NIH HHS R21 AI104268NIAID NIH HHS R21AI104268NIAID NIH HHS T32 AI007637NIAID NIH HHS T32 AI060519
6 · The paper itself

Abstract

unlabelledThe pathogenesis of accelerated liver damage in subjects coinfected with hepatitis C virus (HCV) and human immunodeficiency virus type 1 (HIV-1) remains largely unknown. Recent studies suggest that ongoing chronic liver inflammation is responsible for the liver injury in HCV-infected patients. We aimed to determine whether HIV-1 coinfection altered intrahepatic inflammatory profiles in HCV infection, thereby hastening liver damage. We used a real-time RT-PCR-based array to comparatively analyze intrahepatic inflammation gene profiles in liver biopsy specimens from HCV-infected (n = 16), HCV/HIV-1-coinfected (n = 8) and uninfected (n = 8) individuals. We then used human hepatocytes to study the molecular mechanisms underlying alternations of the inflammatory profiles. Compared with uninfected individuals, HCV infection and HCV/HIV-1 coinfection markedly altered expression of 59.5% and 50.0% of 84 inflammation-related genes tested, respectively. Among these genes affected, HCV infection up-regulated the expression of 24 genes and down-regulated the expression of 26 genes, whereas HCV/HIV-1 coinfection up-regulated the expression of 21 genes and down-regulated the expression of 21 genes. Compared with HCV infection, HCV/HIV-1 coinfection did not dramatically affect intrahepatic gene expression profiles of cytokines and their receptors, but profoundly altered expression of several chemokine genes including up-regulation of the CXCR3-associated chemokines. Human hepatocytes produced these chemokines in response to virus-related microbial translocation, viral protein stimulation, and antiviral immune responses.

conclusionsHIV-1 coinfection profoundly alters intrahepatic chemokine but not cytokine profiles in HCV-infected subjects. The altered chemokines may orchestrate the tissue-specific and cell-selective trafficking of immune cells and autoimmunity to accelerate liver disease in HCV/HIV-1 coinfection.

Indexed as

AdolescentAdultAgedChemokinesCohort StudiesCoinfectionDemographyFemaleGene Expression RegulationHepatitis CHepatocytesHIV InfectionsHumansInflammation MediatorsLipopolysaccharidesLiverChemokinesCXCR3 protein, humanInflammation MediatorsLipopolysaccharidesReceptors, CXCR3RNA, Messenger

Identifiers

PMID24516541
PMCPMC3916319
OpenAlexW2086861294

What OpenQuestion holds

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Registered trials

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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.