Sex-Based Differences in Human Immunodeficiency Virus Type 1 Reservoir Activity and Residual Immune Activation.
Adult
Anti-HIV Agents
/ therapeutic use
CD4-Positive T-Lymphocytes
/ metabolism
CD8-Positive T-Lymphocytes
/ metabolism
DNA, Viral
/ blood
Female
HIV Infections
/ drug therapy
HIV-1
Humans
Lymphocyte Activation
Male
Middle Aged
Programmed Cell Death 1 Receptor
/ blood
Prospective Studies
RNA, Viral
/ blood
Receptors, CCR5
/ metabolism
Sex Factors
Viral Load
HIV-1
cure
immune activation
reservoir
sex differences
Journal
The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675
Informations de publication
Date de publication:
15 03 2019
15 03 2019
Historique:
received:
01
08
2018
accepted:
26
10
2018
pubmed:
30
10
2018
medline:
14
1
2020
entrez:
30
10
2018
Statut:
ppublish
Résumé
Plasma human immunodeficiency virus type 1 (HIV-1) RNA levels in women are lower early in untreated HIV-1 infection compared with those in men, but women have higher T-cell activation and faster disease progression when adjusted for viral load. It is not known whether these sex differences persist during effective antiretroviral therapy (ART), or whether they would be relevant for the evaluation and implementation of HIV-1 cure strategies. We prospectively enrolled a cohort of reproductive-aged women and matched men on suppressive ART and measured markers of HIV-1 persistence, residual virus activity, and immune activation. The frequency of CD4+ T cells harboring HIV-1 DNA was comparable between the sexes, but there was higher cell-associated HIV-1 RNA, higher plasma HIV-1 (single copy assay), and higher T-cell activation and PD-1 expression in men compared with women. These sex-related differences in immune phenotype and HIV-1 persistence on ART have significant implications for the design and measurement of curative interventions.
Identifiants
pubmed: 30371873
pii: 5146028
doi: 10.1093/infdis/jiy617
pmc: PMC6784502
doi:
Substances chimiques
Anti-HIV Agents
0
CCR5 protein, human
0
DNA, Viral
0
PDCD1 protein, human
0
Programmed Cell Death 1 Receptor
0
RNA, Viral
0
Receptors, CCR5
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1084-1094Subventions
Organisme : NIAID NIH HHS
ID : P30 AI027763
Pays : United States
Organisme : NIAID NIH HHS
ID : P30 AI036219
Pays : United States
Organisme : NIAID NIH HHS
ID : K08 AI116344
Pays : United States
Organisme : NIAID NIH HHS
ID : K24 AI069994
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000004
Pays : United States
Organisme : NIAID NIH HHS
ID : R24 AI067039
Pays : United States
Organisme : NCI NIH HHS
ID : HHSN261200800001E
Pays : United States
Informations de copyright
© The Author(s) 2018. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.
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