TLR7 dosage polymorphism shapes interferogenesis and HIV-1 acute viremia in women.


Journal

JCI insight
ISSN: 2379-3708
Titre abrégé: JCI Insight
Pays: United States
ID NLM: 101676073

Informations de publication

Date de publication:
18 06 2020
Historique:
received: 30 12 2019
accepted: 06 05 2020
entrez: 20 6 2020
pubmed: 20 6 2020
medline: 9 6 2021
Statut: epublish

Résumé

Type I IFN (IFN-I) production by plasmacytoid DCs (pDCs) occurs during acute HIV-1 infection in response to TLR7 stimulation, but the role of pDC-derived IFN-I in controlling or promoting HIV-1 infection is ambiguous. We report here a sex-biased interferogenic phenotype for a frequent single-nucleotide polymorphism of human TLR7, rs179008, displaying an impact on key parameters of acute HIV-1 infection. We show allele rs179008 T to determine lower TLR7 protein abundance in cells from women, specifically - likely by diminishing TLR7 mRNA translation efficiency through codon usage. The hypomorphic TLR7 phenotype is mirrored by decreased TLR7-driven IFN-I production by female pDCs. Among women from the French ANRS PRIMO cohort of acute HIV-1 patients, carriage of allele rs179008 T associated with lower viremia, cell-associated HIV-1 DNA, and CXCL10 (IP-10) plasma concentrations. RNA viral load was decreased by 0.85 log10 (95% CI, -1.51 to -0.18) among T/T homozygotes, who also exhibited a lower frequency of acute symptoms. TLR7 emerges as an important control locus for acute HIV-1 viremia, and the clinical phenotype for allele rs179008 T, carried by 30%-50% of European women, supports a beneficial effect of toning down TLR7-driven IFN-I production by pDCs during acute HIV-1 infection.

Identifiants

pubmed: 32554924
pii: 136047
doi: 10.1172/jci.insight.136047
pmc: PMC7406249
doi:
pii:

Substances chimiques

Interferon-alpha 0
TLR7 protein, human 0
Toll-Like Receptor 7 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

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Auteurs

Pascal Azar (P)

Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, UMR 1043 INSERM, CNRS, Toulouse, France.

José Enrique Mejía (JE)

Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, UMR 1043 INSERM, CNRS, Toulouse, France.

Claire Cenac (C)

Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, UMR 1043 INSERM, CNRS, Toulouse, France.

Arnoo Shaiykova (A)

Centre de Recherche en Epidémiologie et Santé des Populations (CESP), Université Paris-Sud, Université Paris-Saclay, INSERM, Le Kremlin-Bicêtre, France.

Ali Youness (A)

Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, UMR 1043 INSERM, CNRS, Toulouse, France.

Sophie Laffont (S)

Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, UMR 1043 INSERM, CNRS, Toulouse, France.

Asma Essat (A)

Centre de Recherche en Epidémiologie et Santé des Populations (CESP), Université Paris-Sud, Université Paris-Saclay, INSERM, Le Kremlin-Bicêtre, France.

Jacques Izopet (J)

Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, UMR 1043 INSERM, CNRS, Toulouse, France.
Laboratoire de Virologie, CHU Purpan, Toulouse, France.

Caroline Passaes (C)

Institut Pasteur, Unité HIV Inflammation et Persistance, Paris, France.

Michaela Müller-Trutwin (M)

Institut Pasteur, Unité HIV Inflammation et Persistance, Paris, France.

Pierre Delobel (P)

Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, UMR 1043 INSERM, CNRS, Toulouse, France.
Service des Maladies Infectieuses et Tropicales, CHU Purpan, Toulouse, France.

Laurence Meyer (L)

Centre de Recherche en Epidémiologie et Santé des Populations (CESP), Université Paris-Sud, Université Paris-Saclay, INSERM, Le Kremlin-Bicêtre, France.

Jean-Charles Guéry (JC)

Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, UMR 1043 INSERM, CNRS, Toulouse, France.

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Classifications MeSH