The Journal of general virology 2016 8 16() doi 10.1099/jgv.0.000577
During HIV infection sCD14 is up-regulated as a consequence of pathological disruption of the gut epithelial barrier which results in increased microbial translocation. Also in HCV infected patients with advanced liver fibrosis, increased levels of sCD14 have been reported. Since the liver plays an important role in clearance of translocated bacterial products, hepatic fibrosis may negatively affect clearance, and thus contribute to higher sCD14 levels. Chimpanzees (Pan troglodytes) infected with hepatitis C virus typically show no signs of liver fibrosis. Here, we have tested the hypothesis that increased levels of sCD14 occur in the absence of hepatic fibrosis or microbial translocation in chimpanzees chronically infected with HCV. sCD14 was up-regulated in both HIV/SIV and HCV infected chimpanzees. In HIV/SIV infected chimpanzees, intestinal fatty acid binding protein (I-FABP), a marker for gut perturbation, and LPS-binding-protein and LPS core antibodies, confirm that sCD14 up-regulation was caused by increased microbial translocation. In HCV infected chimpanzees, no evidence was found for increased microbial translocation, despite up-regulation of sCD14. Additionally, the impact of liver fibrosis on microbial translocation was addressed by direct comparison of chimpanzees with a high HCV load and human patients with advanced fibrosis. These data suggest that only in a small minority of the HCV patients, hepatic fibrosis corroborates microbial translocation.