[10] AFC8-hu HSC/Hep mice supported HCV infection in the liver and generated anti-HCV human T-cell response. Additionally, HCV infection see more induced hepatitis and liver fibrosis, which correlated with activation of human hepatic stellate cells and expression of human fibrogenic genes (Fig. 1 and Washburn et al.[10]). The mechanism of human-specific fibrosis induction in the chimeric liver is not clear. The AFC8-hu mouse provides an excellent model to study how HCV or HBV infection induces human liver fibrosis in vivo. The humanized AFC8 mouse is the first and only in vivo small animal model to recapitulate HCV infection, immune responses, and its associated liver disease, as observed in

humans. It also supports infection of both HCV and human immunodeficiency virus (HIV) 1. Because HIV-1 coinfection has been reported to significantly exacerbate HCV-related liver diseases, the AFC8-hu HSC/Hep mouse allows investigation of

HCV and HIV-1 coinfection in vivo.[45, 46] However, the human liver engraftment in the current AFC8-hu mice (∼15%) is relatively low. It is difficult to support significant replication of HCV to show detectable viremia in the blood. Thus, it is important to improve it, either by more efficient depletion of mouse liver cells or by enhancing human liver cell proliferation and survival, to support efficient HCV infection. HBV infection is more efficient in other humanized mouse models with chimeric human liver. Consistently,

long-term HBV infection is supported in AFC8-hu HSC/Hep mice, associated with similar immunopathogenesis and liver diseases check details (Bility and Su, unpubl. data, 2012). It is thus critical that the current AFC8-hu L-gulonolactone oxidase mouse model is improved that will support robust HBV/HCV infection, immunopathogenesis, and liver diseases, including fibrosis, cirrhosis, and cancer. The models will play a critical role in elucidating immune mechanisms of HBV/HCV-induced liver diseases, as well as in developing novel therapeutic strategies to treat HBV/HCV infection. This work was supported in part by a UNC UCRF innovation grant, by NIH: UNC SPORE (AI076142, AA018009) grants (L.S.), and by UNC Lineberger Comprehensive Cancer Center and UNC Infectious Disease Pathogenesis Postdoctoral Training grants (M.T.B.). The authors have no potential conflicts of interest to declare. “
“Although perihepatic lymph node enlargement (PLNE) is known as a common finding in chronic liver disease, it can be found occasionally at a general health examination. We aimed to clarify the clinical significance of PLNE in general. Between January 2008 and December 2011, 4234 subjects were enrolled, who underwent a general health examination at the University of Tokyo Hospital. PLNE was observed in 69 (1.6%) subjects, among whom 17 (0.4%) had liver disorders and 13 (0.3%) had malignancy, one of whom had both. No disorders were determined in the remaining 40 subjects (0.9%).