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PLoS One. 2017 Sep 13;12(9):e0181004. doi: 10.1371/journal.pone.0181004. eCollection 2017.

The effect of HIV infection and HCV viremia on inflammatory mediators and hepatic injury-The Women's Interagency HIV Study.

Author information

1
Blood Systems Research Institute, San Francisco, California, United States of America.
2
Department of Laboratory Medicine, University of California San Francisco, California, United States of America.
3
Department of Surgery, UCSF, San Francisco, California, United States of America.
4
Department of Medicine, UCSF, San Francisco, California, United States of America.
5
Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, United States of America.
6
CORE Center, Stroger Hospital of Cook County, Chicago, Illinois, United States of America.
7
Department of Medicine, Division of Infectious Diseases, Weill Cornell Medical College, New York, New York, United States of America.
8
Department of Medicine, SUNY Downstate, Brooklyn, New York, United States of America.
9
Department of Pathology and Medicine, George Washington University Medical Center, Washington DC, United States of America.
10
Department of Pediatrics, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
11
Department of Pharmacology, UCSF, San Francisco, California, United States of America.

Abstract

Hepatitis C virus infection induces inflammation and while it is believed that HIV co-infection enhances this response, HIV control may reduce inflammation and liver fibrosis in resolved or viremic HCV infection. Measurement of systemic biomarkers in co-infection could help define the mechanism of inflammation on fibrosis and determine if HIV control reduces liver pathology. A nested case-control study was performed to explore the relationship of systemic biomarkers of inflammation with liver fibrosis in HCV viremic and/or seropositive women with and without HIV infection. Serum cytokines, chemokines, growth factors and cell adhesion molecules were measured in HIV uninfected (HIV-, n = 18), ART-treated HIV-controlled (ARTc, n = 20), uncontrolled on anti-retroviral therapy (ARTuc, n = 21) and elite HIV controllers (Elite, n = 20). All were HCV seroreactive and had either resolved (HCV RNA-; <50IU/mL) or had chronic HCV infection (HCV RNA+). In HCV and HIV groups, aspartate aminotransferase to platelet ratio (APRI) was measured and compared to serum cytokines, chemokines, growth factors and cell adhesion molecules. APRI correlated with sVCAM, sICAM, IL-10, and IP-10 levels and inversely correlated with EGF, IL-17, TGF-α and MMP-9 levels. Collectively, all HCV RNA+ subjects had higher sVCAM, sICAM and IP-10 compared to HCV RNA-. In the ART-treated HCV RNA+ groups, TNF-α, GRO, IP-10, MCP-1 and MDC were higher than HIV-, Elite or both. In ARTuc, FGF-2, MPO, soluble E-selectin, MMP-9, IL-17, GM-CSF and TGF-α are lower than HIV-, Elite or both. Differential expression of soluble markers may reveal mechanisms of pathogenesis or possibly reduction of fibrosis in HCV/HIV co-infection.

PMID:
28902848
PMCID:
PMC5597129
DOI:
10.1371/journal.pone.0181004
[Indexed for MEDLINE]
Free PMC Article

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