Evidence map›Paper›PMID 27509048›Full record

ArticlePLoS pathogens2016

Elevated Basal Pre-infection CXCL10 in Plasma and in the Small Intestine after Infection Are Associated with More Rapid HIV/SIV Disease Onset.

Mickaël J Ploquin, Yoann Madec, Armanda Casrouge, Nicolas Huot, Caroline Passaes, Camille Lécuroux, Asma Essat, Faroudy Boufassa, Béatrice Jacquelin, Simon P Jochems and 20 more

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03137797 (Cohort of Patients Naive of Antiretroviral Treatment at Enrollment), which is not on this map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.3field-weighted citation impact, top 5% 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.

NCT03137797 completednot on this map

Cohort of Patients Naive of Antiretroviral Treatment at Enrollment

TypeobservationalSponsorANRS, Emerging Infectious DiseasesRan2004 to 2016Enrolled800ConditionsHIV Infection
3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Tripterygium wilfordii Hook F accelerates CD4Frontiers in pharmacology · 2026
    Article
  4. Article
  5. Under the Radar: Immune Evasion, Pathogenesis and Control of HIV Infection.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Effects of Morphine on Gp120-induced Neuroinflammation Under Immunocompetent Vs. Immunodeficient Conditions.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Effects of HIV gp120 on Neuroinflammation in Immunodeficient vs. Immunocompetent States.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021
    Article
  19. Article
  20. Role of NKG2a/ciScience · 2021
    Article
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

30 authors at 5 institutions in 2 countries.

Mickaël J PloquinInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Yoann MadecInstitut Pasteur, Département de infection et épidémiologie, Unité de Recherche et d'Expertise Epidémiologie des Maladies Emergentes, Paris, France.ORCID 0000-0002-6201-1261
Armanda CasrougeInstitut Pasteur, Département d'immunologie, Unité Immunobiologie des cellules dendritiques, INSERM U818, Paris, France.
Nicolas HuotInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Caroline PassaesInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Camille LécurouxINSERM CESP U1018, Université Paris Saclay, Université Paris Sud, AP-HP, Le Kremlin-Bicêtre, France.
Asma EssatINSERM CESP U1018, Université Paris Saclay, Université Paris Sud, AP-HP, Le Kremlin-Bicêtre, France.
Faroudy BoufassaINSERM CESP U1018, Université Paris Saclay, Université Paris Sud, AP-HP, Le Kremlin-Bicêtre, France.
Béatrice JacquelinInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Simon P JochemsInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Gaël PetitjeanInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Mathieu AnginInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Kathleen GärtnerInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Thalía Garcia-TellezInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Nicolas NoëlCommissariat à l'Energie atomique et aux énergies alternatives, Division IMVA/IDMIT/IMETI/SIV CEA, Fontenay-aux-Roses, France.ORCID 0000-0003-4055-617X
Thijs BooimanAcademisch Medisch Centrum, Laboratory of Viral Immune Pathogenesis, Amsterdam The Netherlands.
Brigitte D Boeser-NunninkAcademisch Medisch Centrum, Laboratory of Viral Immune Pathogenesis, Amsterdam The Netherlands.
Pierre RoquesCommissariat à l'Energie atomique et aux énergies alternatives, Division IMVA/IDMIT/IMETI/SIV CEA, Fontenay-aux-Roses, France.
Asier Saez-CirionInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Bruno VaslinCommissariat à l'Energie atomique et aux énergies alternatives, Division IMVA/IDMIT/IMETI/SIV CEA, Fontenay-aux-Roses, France.
Nathalie Dereudre-BosquetCommissariat à l'Energie atomique et aux énergies alternatives, Division IMVA/IDMIT/IMETI/SIV CEA, Fontenay-aux-Roses, France.
Françoise Barré-SinoussiInstitut Pasteur, Département de Virologie, Unité Régulation des infections rétrovirales, Paris, France.
Mathilde GhislainINSERM CESP U1018, Université Paris Saclay, Université Paris Sud, AP-HP, Le Kremlin-Bicêtre, France.
Christine RouziouxCentre Hospitalier Universitaire Necker-Hôpitaux de Paris, Laboratoire de Virologie, Paris, France.
Olivier LambotteCommissariat à l'Energie atomique et aux énergies alternatives, Division IMVA/IDMIT/IMETI/SIV CEA, Fontenay-aux-Roses, France.
Matthew L AlbertInstitut Pasteur, Département d'immunologie, Unité Immunobiologie des cellules dendritiques, INSERM U818, Paris, France.
Cécile GoujardCommissariat à l'Energie atomique et aux énergies alternatives, Division IMVA/IDMIT/IMETI/SIV CEA, Fontenay-aux-Roses, France.
Neeltje KootstraAcademisch Medisch Centrum, Laboratory of Viral Immune Pathogenesis, Amsterdam The Netherlands.
Laurence MeyerINSERM CESP U1018, Université Paris Saclay, Université Paris Sud, AP-HP, Le Kremlin-Bicêtre, France.
Michaela C Müller-TrutwinInstitut Pasteur, Département de Virologie, Unité HIV, Inflammation et Persistance, Paris, France.
Institut Pasteur · FRUniversité Paris-Sud · FRAmsterdam UMC Location University of Amsterdam · NLInserm · FRDélégation Paris 5 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated blood CXCL10/IP-10 levels during primary HIV-1 infection (PHI) were described as an independent marker of rapid disease onset, more robust than peak viremia or CD4 cell nadir. IP-10 enhances the recruitment of CXCR3+ cells, which include major HIV-target cells, raising the question if it promotes the establishment of viral reservoirs. We analyzed data from four cohorts of HIV+ patients, allowing us to study IP-10 levels before infection (Amsterdam cohort), as well as during controlled and uncontrolled viremia (ANRS cohorts). We also addressed IP-10 expression levels with regards to lymphoid tissues (LT) and blood viral reservoirs in patients and non-human primates. Pre-existing elevated IP-10 levels but not sCD63 associated with rapid CD4 T-cell loss upon HIV-1 infection. During PHI, IP-10 levels and to a lesser level IL-18 correlated with cell-associated HIV DNA, while 26 other inflammatory soluble markers did not. IP-10 levels tended to differ between HIV controllers with detectable and undetectable viremia. IP-10 was increased in SIV-exposed aviremic macaques with detectable SIV DNA in tissues. IP-10 mRNA was produced at higher levels in the small intestine than in colon or rectum. Jejunal IP-10+ cells corresponded to numerous small and round CD68neg cells as well as to macrophages. Blood IP-10 response negatively correlated with RORC (Th17 marker) gene expression in the small intestine. CXCR3 expression was higher on memory CD4+ T cells than any other immune cells. CD4 T cells from chronically infected animals expressed extremely high levels of intra-cellular CXCR3 suggesting internalization after ligand recognition. Elevated systemic IP-10 levels before infection associated with rapid disease progression. Systemic IP-10 during PHI correlated with HIV DNA. IP-10 production was regionalized in the intestine during early SIV infection and CD68+ and CD68neg haematopoietic cells in the small intestine appeared to be the major source of IP-10.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell SeparationChemokine CXCL10Disease ProgressionFlow CytometryHIV-1HIV InfectionsHumansImmunohistochemistryIntestine, SmallMacacaPolymerase Chain ReactionSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusViral LoadChemokine CXCL10

Identifiers

PMID27509048
PMCPMC4980058
OpenAlexW2491803890

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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.