Host genetic and immune factors drive evasion of HIV-1 pathogenesis in viremic non-progressors.

CCR5 CTL activation HIV reservoir HIV-1 pathogenesis Translation to patients VNP interferon single-cell RNA sequencing tryptophan viremic non-progressor zonulin

Journal

Med (New York, N.Y.)
ISSN: 2666-6340
Titre abrégé: Med
Pays: United States
ID NLM: 101769215

Informations de publication

Date de publication:
09 Oct 2024
Historique:
received: 13 03 2024
revised: 03 06 2024
accepted: 13 09 2024
medline: 17 10 2024
pubmed: 17 10 2024
entrez: 16 10 2024
Statut: aheadofprint

Résumé

Viremic non-progressors (VNPs) represent an exceptional and uncommon subset of people with HIV-1, characterized by the remarkable preservation of normal CD4 We implemented a novel single-cell and multiomics approach to comprehensively characterize viral, genomic, transcriptomic, and metabolomic factors driving this exceedingly rare disease phenotype in 16 VNPs and 29 HIV+ progressors. Genetic predisposition to the VNP phenotype was evidenced by a higher prevalence of CCR5Δ32 heterozygosity, which was associated with lower levels of CCR5 expression and a lower frequency of infected cells in peripheral circulation. We also observed reduced levels of plasma markers of intestinal disruption and attenuated interferon responses in VNPs. These factors potentially drive the other phenotypic traits of immune preservation in this population, including the unaltered tryptophan metabolic profile, reduced activation of cytotoxic lymphocytes, and reduced bystander CD4 In summary, our comprehensive analysis identified intricate factors collectively associated with the unique immunovirological equilibrium in VNPs, shedding light on potential avenues for therapeutic exploration in managing HIV pathogenesis. The work was supported by funding from the Spanish Ministry of Science and Innovation and the National Institutes of Health (NIH).

Sections du résumé

BACKGROUND BACKGROUND
Viremic non-progressors (VNPs) represent an exceptional and uncommon subset of people with HIV-1, characterized by the remarkable preservation of normal CD4
METHODS METHODS
We implemented a novel single-cell and multiomics approach to comprehensively characterize viral, genomic, transcriptomic, and metabolomic factors driving this exceedingly rare disease phenotype in 16 VNPs and 29 HIV+ progressors.
FINDINGS RESULTS
Genetic predisposition to the VNP phenotype was evidenced by a higher prevalence of CCR5Δ32 heterozygosity, which was associated with lower levels of CCR5 expression and a lower frequency of infected cells in peripheral circulation. We also observed reduced levels of plasma markers of intestinal disruption and attenuated interferon responses in VNPs. These factors potentially drive the other phenotypic traits of immune preservation in this population, including the unaltered tryptophan metabolic profile, reduced activation of cytotoxic lymphocytes, and reduced bystander CD4
CONCLUSIONS CONCLUSIONS
In summary, our comprehensive analysis identified intricate factors collectively associated with the unique immunovirological equilibrium in VNPs, shedding light on potential avenues for therapeutic exploration in managing HIV pathogenesis.
FUNDING BACKGROUND
The work was supported by funding from the Spanish Ministry of Science and Innovation and the National Institutes of Health (NIH).

Identifiants

pubmed: 39413785
pii: S2666-6340(24)00374-X
doi: 10.1016/j.medj.2024.09.007
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests H.H. is co-founder and shareholder of Omniscope, a member of the scientific advisory boards of Nanostring and MiRXES, and consultant to Moderna and Singularity.

Auteurs

Ángel Bayón-Gil (Á)

IrsiCaixa, Badalona, Spain.

Inmaculada Hernández (I)

Single Cell Genomics Group, CNAG-CRG, National Centre for Genomic Analysis (CNAG), Barcelona, Spain.

Judith Dalmau (J)

IrsiCaixa, Badalona, Spain.

Juan C Nieto (JC)

Single Cell Genomics Group, CNAG-CRG, National Centre for Genomic Analysis (CNAG), Barcelona, Spain.

Víctor Urrea (V)

IrsiCaixa, Badalona, Spain.

Lidia Garrido-Sanz (L)

IrsiCaixa, Badalona, Spain.

Ginevra Caratú (G)

Single Cell Genomics Group, CNAG-CRG, National Centre for Genomic Analysis (CNAG), Barcelona, Spain.

Maria C García-Guerrero (MC)

IrsiCaixa, Badalona, Spain.

Cristina Gálvez (C)

IrsiCaixa, Badalona, Spain.

María Salgado (M)

IrsiCaixa, Badalona, Spain; Germans Trias i Pujol Research Institute, Badalona, Spain; CIBERINFEC, Instituto de Salud Carlos III, Madrid, Spain.

Itziar Erkizia (I)

IrsiCaixa, Badalona, Spain.

Fernando Laguía (F)

IrsiCaixa, Badalona, Spain.

Patricia Resa-Infante (P)

IrsiCaixa, Badalona, Spain; Germans Trias i Pujol Research Institute, Badalona, Spain; CIBERINFEC, Instituto de Salud Carlos III, Madrid, Spain; Infectious Diseases and Immunity Department, University of Vic-Central University of Catalonia, Vic, Spain.

Marta Massanella (M)

IrsiCaixa, Badalona, Spain; CIBERINFEC, Instituto de Salud Carlos III, Madrid, Spain.

Raúl Tonda (R)

CNAG-CRG, National Centre for Genomic Analysis (CNAG), Barcelona, Spain.

Jordi Morata (J)

CNAG-CRG, National Centre for Genomic Analysis (CNAG), Barcelona, Spain.

Kai Ying Hong (KY)

The Wistar Institute, Philadelphia, PA, USA.

Jane Koshy (J)

The Wistar Institute, Philadelphia, PA, USA.

Aaron R Goldman (AR)

The Wistar Institute, Philadelphia, PA, USA.

Leila Giron (L)

The Wistar Institute, Philadelphia, PA, USA.

Mohamed Abdel-Mohsen (M)

The Wistar Institute, Philadelphia, PA, USA.

Holger Heyn (H)

Single Cell Genomics Group, CNAG-CRG, National Centre for Genomic Analysis (CNAG), Barcelona, Spain.

Javier Martinez-Picado (J)

IrsiCaixa, Badalona, Spain; Germans Trias i Pujol Research Institute, Badalona, Spain; CIBERINFEC, Instituto de Salud Carlos III, Madrid, Spain; Infectious Diseases and Immunity Department, University of Vic-Central University of Catalonia, Vic, Spain; ICREA, Catalan Institution for Research and Advanced Studies, Barcelona, Spain. Electronic address: jmpicado@irsicaixa.es.

Maria C Puertas (MC)

IrsiCaixa, Badalona, Spain; Germans Trias i Pujol Research Institute, Badalona, Spain; CIBERINFEC, Instituto de Salud Carlos III, Madrid, Spain. Electronic address: mcpuertas@irsicaixa.es.

Classifications MeSH