Evidence map›Paper›PMID 40709192›Full record

ArticleFrontiers in immunology2025

Patterns of inflammation and immune activation by coreceptor use in people living with HIV-1.

Francisco Xavier Guerra-Castillo, Sandra Pinto-Cardoso, Santiago Ávila-Ríos, Monserrat Chávez-Torres, Amy Peralta-Prado, Carolina González-Torres, Javier Gaytán-Cervantes, Brenda Requena-Benitez, Dafne Díaz-Rivera, Carmen Alaez-Verson and 2 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

12 authors.

Francisco Xavier Guerra-CastilloUnidad de Investigación Médica en Inmunología e Infectología, Hospital de Infectología "Dr. Daniel Méndez Hernández", Centro Médico Nacional La Raza, Instituto Mexicano del Seguro Social (IMSS), Ciudad de México, Mexico.
Sandra Pinto-CardosoCentro de Investigación en Enfermedades Infecciosas, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México, Mexico.
Santiago Ávila-RíosCentro de Investigación en Enfermedades Infecciosas, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México, Mexico.
Monserrat Chávez-TorresCentro de Investigación en Enfermedades Infecciosas, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México, Mexico.
Amy Peralta-PradoCentro de Investigación en Enfermedades Infecciosas, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México, Mexico.
Carolina González-TorresLaboratorio de Secuenciación, División de Desarrollo de la Investigación en Salud, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, Mexico.
Javier Gaytán-CervantesLaboratorio de Secuenciación, División de Desarrollo de la Investigación en Salud, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, Mexico.
Brenda Requena-BenitezUnidad de Investigación Médica en Inmunología e Infectología, Hospital de Infectología "Dr. Daniel Méndez Hernández", Centro Médico Nacional La Raza, Instituto Mexicano del Seguro Social (IMSS), Ciudad de México, Mexico.
Dafne Díaz-RiveraCentro de Investigación en Enfermedades Infecciosas, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México, Mexico.
Carmen Alaez-VersonLaboratorio de Diagnóstico Genómico, Instituto Nacional de Médicina Genómica (INMEGEN), Ciudad de México, Mexico.
María Concepción Hernández-GarcíaHospital de Infectología "Dr. Daniel Méndez Hernández", Centro Médico Nacional La Raza, Instituto Mexicano del Seguro Social (IMSS), Ciudad de México, Mexico.
Vilma Carolina Bekker-MéndezUnidad de Investigación Médica en Inmunología e Infectología, Hospital de Infectología "Dr. Daniel Méndez Hernández", Centro Médico Nacional La Raza, Instituto Mexicano del Seguro Social (IMSS), Ciudad de México, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Human immunodeficiency virus type 1 (HIV-1) utilizes either the CCR5 (R5) or CXCR4 (X4) coreceptor for host cell entry. Coreceptor switching from R5 to X4 and elevated immune activation have been associated with disease progression. X4-tropic HIV-1 is predominantly observed in the late stage of infection, when the immune environment characterized by chronic activation is optimal for their replication. The aim of this study was to determine viral tropism in late HIV presenters and who have not previously received treatment in Mexico City and its relationship with markers of chronic immune activation. Methods: A cross-sectional study was conducted on 122 people living with HIV (PLWH) recruited from two public health services. Viral tropism was determined using next-generation sequencing (NGS) and the geno2pheno algorithm. Immune activation was assessed through flow cytometry (CD38+, HLA-DR+), and soluble markers (sCD14, sCD163, IL-6) were quantified using enzyme-linked immunosorbent assays (ELISA). Differences in immune activation patterns between R5 and X4 group were explored using Mann-Whitney Wilcoxon test and t-test, and a principal component analysis (PCA). Logistic regression was used to evaluate associations between immune activation profiles and the presence of X4-tropic viruses. Results: Ninety-eight individuals had high-quality V3 loop sequences, 81.6% harbored only R5 variants (R5 group), while 18.4% had mixed R5/X4 populations (X4 group). Most PLWH had CD4+ T cell counts below 200 cells/µL, showing no significant difference between groups. Elevated levels of IL-6 were significantly associated with the R5 group (p = 0.01), while the X4 group showed increased expression of CD38+ and HLA-DR+CD38+ markers, although not statistically significant. Furthermore, IL-6 emerges as a negative predictor for the presence of X4 viruses (OR = 0.06, p = 0.006). Conclusion: R5-tropic viruses are associated with elevated inflammatory responses in early stages, as indicated by higher IL-6 levels, while X4-tropic viruses may contribute to CD4+ T cell depletion through immune activation. Consequently, elevated levels of IL-6 emerge as a negative predictor for the presence of X4 viruses. The relationship between viral tropism and chronic immune activation in HIV-1 infection reflects a complex interplay which appears to be bidirectional.

Indexed as

HIV-1HIV InfectionsInflammationReceptors, CCR5Receptors, CXCR4AdultBiomarkersCross-Sectional StudiesFemaleHumansLymphocyte ActivationMaleMiddle AgedViral TropismBiomarkersCCR5 protein, humanCXCR4 protein, humanReceptors, CCR5Receptors, CXCR4CCR5CD38chronic immune activationCXCR4HIV-1 tropismHLA-DRIL-6next generation sequencing

Identifiers

PMID40709192
PMCPMC12286835

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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.