Evidence map›Paper›PMID 33785040›Full record

ArticleJournal of biomedical science2021

HCV eradication with IFN-based therapy does not completely restore gene expression in PBMCs from HIV/HCV-coinfected patients.

Óscar Brochado, Isidoro Martínez, Juan Berenguer, Luz Medrano, Juan González-García, María Ángeles Jiménez-Sousa, Ana Carrero, Víctor Hontañón, Jordi Navarro, Josep M Guardiola and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
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  3. UnravelingFrontiers in oncology · 2024
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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

13 authors at 7 institutions in 1 country.

Óscar BrochadoUnidad de Infección Viral E Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda), Carretera Majadahonda-Pozuelo, Km 2.2, 28220, MajadahondaMadrid, Spain.
Isidoro MartínezUnidad de Infección Viral E Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda), Carretera Majadahonda-Pozuelo, Km 2.2, 28220, MajadahondaMadrid, Spain. imago@isciii.es.
Juan BerenguerUnidad de Enfermedades Infecciosas/VIH, Hospital General Universitario "Gregorio Marañón", Madrid, Spain.
Luz MedranoUnidad de Infección Viral E Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda), Carretera Majadahonda-Pozuelo, Km 2.2, 28220, MajadahondaMadrid, Spain.
Juan González-GarcíaUnidad de VIH, Servicio de Medicina Interna, Hospital Universitario "La Paz", Madrid, Spain.
María Ángeles Jiménez-SousaUnidad de Infección Viral E Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda), Carretera Majadahonda-Pozuelo, Km 2.2, 28220, MajadahondaMadrid, Spain.
Ana CarreroUnidad de Enfermedades Infecciosas/VIH, Hospital General Universitario "Gregorio Marañón", Madrid, Spain.
Víctor HontañónUnidad de VIH, Servicio de Medicina Interna, Hospital Universitario "La Paz", Madrid, Spain.
Jordi NavarroServicio de Enfermedades Infecciosas, Hospital Universitari Vall D'Hebron, Barcelona, Spain.
Josep M GuardiolaHospital Santa Creu I Sant Pau, Barcelona, Spain.
Amanda Fernández-Rodríguez *Unidad de Infección Viral E Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda), Carretera Majadahonda-Pozuelo, Km 2.2, 28220, MajadahondaMadrid, Spain.
Salvador Resino *Unidad de Infección Viral E Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda), Carretera Majadahonda-Pozuelo, Km 2.2, 28220, MajadahondaMadrid, Spain. sresino@isciii.es.ORCID http://orcid.org/0000-0001-8783-0450
GESIDA Study Group
Hospital de Sant Pau · ESInstituto de Salud Carlos III · ESVall d'Hebron Hospital Universitari · ESHospital General Universitario Gregorio Marañón · ESHospital Universitario La Paz · ESHospital La Paz Institute for Health Research · ESVall d'Hebron Institut de Recerca · ES

Funding

Instituto de Salud Carlos III PI17/00657Instituto de Salud Carlos III PI17/00903Instituto de Salud Carlos III PI18CIII/00020Instituto de Salud Carlos III PI20/00507Instituto de Salud Carlos III PI20CIII/00004Instituto de Salud Carlos III RD16/0025/0017Instituto de Salud Carlos III RD16CIII/0002/0002Instituto de Salud Carlos III (ES) PI17CIII/00003Instituto de Salud Carlos III (ES) PI20/00474Instituto de Salud Carlos III (ES) RD16/0025/0018
6 · The paper itself

Abstract

objectiveTo evaluate the impact of hepatitis C virus (HCV) elimination via interferon (IFN)-based therapy on gene expression profiles related to the immune system in HIV/HCV-coinfected patients.

methodsWe conducted a prospective study in 28 HIV/HCV-coinfected patients receiving IFN-based therapy at baseline (HIV/HCV-b) and week 24 after sustained virological response (HIV/HCV-f). Twenty-seven HIV-monoinfected patients (HIV-mono) were included as a control. RNA-seq analysis was performed on peripheral blood mononuclear cells (PBMCs). Genes with a fold-change (FC) ≥ 1.5 (in either direction) and false discovery rate (FDR) ≤ 0.05 were identified as significantly differentially expressed (SDE).

resultsHIV/HCV-b showed six SDE genes compared to HIV-mono group, but no significantly enriched pathways were observed. For HIV/HCV-f vs. HIV/HCV-b, we found 58 SDE genes, 34 upregulated and 24 downregulated in the HIV/HCV-f group. Of these, the most overexpressed were CXCL2, PDCD6IP, ATP5B, IGSF9, RAB26, and CSRNP1, and the most downregulated were IFI44 and IFI44L. These 58 SDE genes revealed two significantly enriched pathways (FDR < 0.05), one linked to Epstein-Barr virus infection and another related to p53 signaling. For HIV/HCV-f vs. HIV-mono group, we found 44 SDE genes that revealed 31 enriched pathways (FDR < 0.05) related to inflammation, cancer/cell cycle alteration, viral and bacterial infection, and comorbidities associated with HIV/HCV-coinfection. Five genes were overrepresented in most pathways (JUN, NFKBIA, PIK3R2, CDC42, and STAT3).

conclusionHIV/HCV-coinfected patients who eradicated hepatitis C with IFN-based therapy showed profound gene expression changes after achieving sustained virological response. The altered pathways were related to inflammation and liver-related complications, such as non-alcoholic fatty liver disease and hepatocellular carcinoma, underscoring the need for active surveillance for these patients.

Indexed as

Gene ExpressionAdultCoinfectionFemaleHepacivirusHepatitis CHIVHIV InfectionsHumansInterferonsLeukocytes, MononuclearMaleMiddle AgedInterferonsGene expressionHCV clearanceHIV/HCV coinfectionImmune systemInterferon therapyPBMCs

Identifiers

PMID33785040
PMCPMC8010945
OpenAlexW3149892777

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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.