Reversal of hepatitis B virus‐induced immune tolerance by an immunostimulatory 3p‐HBx‐siRNAs in a retinoic acid inducible gene I–dependent manner

Qiuju Han, Cai Zhang, Jian Zhang, Zhigang Tian – 30 June 2011 – It is extensively accepted that hepatitis B virus (HBV) escapes from innate immunity by inhibiting type I interferon (IFN) production, but efficient intervention to reverse the immune tolerance is still not achieved.

Genetic variation in the interleukin‐28B gene is not associated with fibrosis progression in patients with chronic hepatitis C and known date of infection

Francesco Marabita, Alessio Aghemo, Stella De Nicola, Maria G. Rumi, Cristina Cheroni, Rossana Scavelli, Marco Crimi, Roberta Soffredini, Sergio Abrignani, Raffaele De Francesco, Massimo Colombo – 30 June 2011 – Polymorphisms in the interleukin‐28B (IL28B) region are associated with spontaneous and treatment‐induced viral clearance in hepatitis C virus (HCV) infection. Nevertheless, it is unknown whether genetic variation at the IL28B locus influences the natural history of chronic HCV infection.

Intercellular nanovesicle‐mediated microRNA transfer: A mechanism of environmental modulation of hepatocellular cancer cell growth

Takayuki Kogure, Wen‐Lang Lin, Irene K. Yan, Chiara Braconi, Tushar Patel – 30 June 2011 – Hepatocellular carcinoma (HCC) is characterized by a propensity for multifocality, growth by local spread, and dysregulation of multiple signaling pathways. These features may be determined by the tumoral microenvironment. The potential of tumor cells to modulate HCC growth and behavior by secreted proteins has been extensively studied. In contrast, the potential for genetic modulation is poorly understood.

Spontaneous repopulation of β‐catenin null livers with β‐catenin‐positive hepatocytes after chronic murine liver injury

Michael D. Thompson, Emily D. Wickline, William B. Bowen, Amy Lu, Sucha Singh, Amalea Misse, Satdarshan P.S. Monga – 30 June 2011 – Prolonged exposure of mice to diet containing 0.1% 3,5‐diethoxycarbonyl‐1,4‐dihydrocollidine (DDC) results in hepatobiliary injury, atypical ductular proliferation, oval cell appearance, and limited fibrosis. Previously, we reported that short‐term ingestion of DDC diet by hepatocyte‐specific β‐catenin conditional knockout (KO) mice led to fewer A6‐positive oval cells than wildtype (WT) littermates.

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