The effect of HIV infection and HCV viremia on inflammatory mediators and hepatic injury—The Women’s Interagency HIV Study

• Published in: PloS one Vol. 12; no. 9; p. e0181004
• Main Authors: Keating, Sheila M., Dodge, Jennifer L., Norris, Philip J., Heitman, John, Gange, Stephen J., French, Audrey L., Glesby, Marshall J., Edlin, Brian R., Latham, Patricia S., Villacres, Maria C., Greenblatt, Ruth M., Peters, Marion G.
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 13.09.2017; Public Library of Science (PLoS)
• Subjects: Adhesion; Adhesion tests; Adult; AIDS-Related Opportunistic Infections - blood; AIDS-Related Opportunistic Infections - virology; Alcohol; Antiretroviral drugs; Aspartate aminotransferase; Biology and Life Sciences; Biomarkers; Case-Control Studies; Cell adhesion; Cell adhesion molecules; Chemokines; Chronic infection; Coinfection - blood; Coinfection - virology; Cytokines; E-selectin; Female; Fibroblast growth factor 2; Fibrosis; Gelatinase B; Granulocyte-macrophage colony-stimulating factor; Growth factors; Hepacivirus - growth & development; Hepatitis; Hepatitis C; Hepatitis C - blood; Hepatitis C - complications; Hepatitis C - virology; Hepatology; HIV; HIV Infections - blood; HIV Infections - complications; HIV Infections - virology; HIV-1 - growth & development; Human immunodeficiency virus; Humans; Infections; Infectious diseases; Inflammation; Inflammation Mediators - blood; Interleukin 10; Interleukin 17; IP-10 protein; Laboratories; Liver; Liver Cirrhosis - blood; Liver Cirrhosis - pathology; Liver Cirrhosis - virology; Medicine; Medicine and Health Sciences; Middle Aged; Monocyte chemoattractant protein 1; Morbidity; Pathogenesis; Ribonucleic acid; RNA; Rodents; Tumor necrosis factor; Viremia; Viremia - blood; Viremia - virology; Viruses; Womens health; New York; San Francisco California; California; United States > US
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0181004

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.