Decreases in markers of monocyte/macrophage activation after hepatitis C eradication in HIV/hepatitis C virus coinfected women.
Journal
AIDS (London, England)
ISSN: 1473-5571
Titre abrégé: AIDS
Pays: England
ID NLM: 8710219
Informations de publication
Date de publication:
15 07 2021
15 07 2021
Historique:
pubmed:
13
3
2021
medline:
7
8
2021
entrez:
12
3
2021
Statut:
ppublish
Résumé
Eradication of hepatitis C virus (HCV) in HIV disease decreases liver and non-liver-related morbidity and mortality. Elevated markers of monocyte/macrophage activation (soluble CD163 and sCD14) are associated with excess non-AIDS morbidity and mortality in HIV. We examined the effect of HCV eradication on these markers in relation to change in hepatic fibrosis. A nested substudy within a longitudinal observational cohort. We studied 126 HIV/HCV-coinfected women successfully treated for HCV, with undetectable HCV RNA at least 12 weeks after therapy completion. sCD163 and sCD14 were measured in serum collected before and after HCV eradication. Results were correlated with changes in markers of hepatic fibrosis. Mean age of participants was 56.3 years, mean CD4+ cell count was 615, and 72% had suppressed HIV RNA. After treatment, sCD163 and sCD14 levels significantly decreased from pre-treatment levels in unadjusted analyses. After adjusting for age, race, hepatic fibrosis status, baseline HCV RNA, CD4 count and HIV RNA status, cigarette smoking, and alcohol use, the decreases in sCD163 and sCD14 remained significant. Decrease in pre-treatment to post-treatment sCD163 were significantly positively correlated with changes in FIB-4 (r = 0.250, P = 0.005) and APRI (r = 0.262, P = 0.003); similarly decrease in sCD14 was significantly positively correlated with changes in FIB-4 (r = 0.333, P = 0.0001) and APRI (r = 0.457, P < 0.0001). HCV eradication is associated with significant reductions in monocyte/macrophage activation markers that correlate with reductions in markers of hepatic fibrosis. These findings support broad access to and early initiation of HCV treatment in order to decrease immune activation and improve health in HIV-infected persons.
Identifiants
pubmed: 33710024
doi: 10.1097/QAD.0000000000002869
pii: 00002030-202107150-00011
pmc: PMC8845487
mid: NIHMS1680493
doi:
Substances chimiques
Biomarkers
0
Types de publication
Journal Article
Observational Study
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1433-1438Subventions
Organisme : NHLBI NIH HHS
ID : U01 HL146241
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI035004
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL146205
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL146192
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL146242
Pays : United States
Organisme : NIA NIH HHS
ID : R21 AG059505
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL146193
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL146194
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL146203
Pays : United States
Organisme : NIAID NIH HHS
ID : P30 AI094189
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL146245
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL146204
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL146202
Pays : United States
Informations de copyright
Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.
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