Sex differences in cytokine profiles during suppressive antiretroviral therapy.


Journal

AIDS (London, England)
ISSN: 1473-5571
Titre abrégé: AIDS
Pays: England
ID NLM: 8710219

Informations de publication

Date de publication:
15 07 2022
Historique:
pubmed: 25 5 2022
medline: 16 7 2022
entrez: 24 5 2022
Statut: ppublish

Résumé

Despite lower plasma HIV RNA levels, women progress faster to AIDS than men. The reasons for these differences are not clear but might be a consequence of an elevated inflammatory response in women. We investigated sex differences in cytokine profiles by measuring the concentrations of 36 cytokines/chemokines by Luminex in blood of women and men (sex at birth) with chronic HIV infection under suppressive therapy. We initially performed a principal component analysis to see if participants clustered by sex, and then fit a partial least squares discriminant analysis (PLS-DA) model where we used cytokines to predict sex at birth. The significance of the difference in nine cytokines with VIP greater than 1 was tested using Wilcoxon test-rank. Further, potential confounding factors were tested by multivariate linear regression models. Overall, we predicted sex at birth in the PLS-DA model with an error rate of approximately 13%. We identified five cytokines, which were significantly higher in women compared with men, namely the pro-inflammatory chemokines CXCL1 (Gro-α), CCL5 (RANTES), CCL3 (MIP-1α), CCL4 (MIP-1β), as well as the T-cell homeostatic factor IL-7. The effect of sex remained significant after adjusting for CD4 + , age, ethnicity, and race for all cytokines, except for CCL3 and race. The observed sex-based differences in cytokines might contribute to higher immune activation in women compared with men despite suppressive therapy. Increased levels of IL-7 in women suggest that homeostatic proliferation may have a differential contribution to HIV reservoir maintenance in female and male individuals. Our study emphasizes the importance of sex-specific studies of viral pathogenesis.

Identifiants

pubmed: 35608113
doi: 10.1097/QAD.0000000000003265
pii: 00002030-202207150-00002
pmc: PMC9283283
mid: NIHMS1800657
doi:

Substances chimiques

Anti-Retroviral Agents 0
Chemokine CCL4 0
Chemokine CCL5 0
Chemokines 0
Cytokines 0
Interleukin-7 0
Macrophage Inflammatory Proteins 0

Types de publication

Journal Article Research Support, U.S. Gov't, Non-P.H.S. Research Support, N.I.H., Intramural Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1215-1222

Subventions

Organisme : NIAID NIH HHS
ID : R56 AI158293
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI147821
Pays : United States
Organisme : NIMH NIH HHS
ID : P30 MH062512
Pays : United States
Organisme : NIAID NIH HHS
ID : P30 AI036214
Pays : United States
Organisme : NIDA NIH HHS
ID : DP2 DA051915
Pays : United States
Organisme : Intramural NIH HHS
ID : Z99 HD999999
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.

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Auteurs

Christophe Vanpouille (C)

Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland.

Alan Wells (A)

Department of Medicine, University of California San Diego, La Jolla, California.

Timothy Wilkin (T)

Weill Cornell Medicine, New York, New York, USA.

Jyoti S Mathad (JS)

Weill Cornell Medicine, New York, New York, USA.

Sheldon Morris (S)

Department of Medicine, University of California San Diego, La Jolla, California.

Leonid Margolis (L)

Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland.

Sara Gianella (S)

Department of Medicine, University of California San Diego, La Jolla, California.

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