부산대학교 도서관

Objectives Chronic hepatitis C virus ( HCV) and HIV viral infections are characterized by systemic inflammation. Yet the relative levels, drivers and correlates of inflammation in these settings are not well defined. Methods Seventy-nine HIV-infected patients who had been receiving antiretroviral therapy ( ART) for more than 2 years and who had suppressed plasma HIV levels (< 50 HIV-1 RNA copies/mL) were included in the study. Two patient groups, HCV-positive/ HIV-positive and HCV-negative/ HIV-positive, and a control group comprised of healthy volunteers ( n = 20) were examined. Markers of systemic inflammation [interleukin ( IL)-6, interferon gamma-induced protein ( IP)-10, soluble tumour necrosis factor receptor-I ( sTNF- RI) and sTNF- RII], monocyte/macrophage activation [soluble CD163 ( sCD163), soluble CD14 and neopterin], intestinal epithelial barrier loss [intestinal fatty acid binding protein (I- FABP) and lipopolysaccharide ( LPS)] and coagulation ( d-dimers) were analysed. CD4 naïve T cells and CD4 recent thymic emigrants ( RTEs) were enumerated. Results Plasma levels of IP-10, neopterin and sCD163 were higher in HCV/ HIV coinfection than in HIV monoinfection and were positively correlated with indices of hepatic damage [aspartate aminotransferase ( AST), alanine aminotransferase ( ALT) and the AST to platelet ratio index ( APRI)]. Levels of I- FABP were comparably increased in HIV monoinfection and HIV/ HCV coinfection but LPS concentrations were highest in HCV/ HIV coinfection, suggesting impaired hepatic clearance of LPS. Plasma HCV levels were not related to any inflammatory indices except sCD163. In coinfected subjects, a previously recognized relationship of CD4 naïve T-cell and RTE counts to hepatocellular injury was defined more mechanistically by an inverse relationship to sCD163. Conclusions Hepatocellular injury in HCV/ HIV coinfection is linked to elevated levels of certain inflammatory cytokines and an apparent failure to clear systemically translocated microbial products. A related decrease in CD4 naïve T cells and RTEs also merits further exploration. [ABSTRACT FROM AUTHOR]