Nasser Semmo, Cheryl L. Day, Scott M. Ward, Michaela Lucas, Gillian Harcourt, Andrew Loughry, Paul Klenerman – 19 April 2005 – Hepatitis C virus (HCV) becomes persistent in the majority of infected individuals. In doing so, the virus evades host adaptive immune responses, although the mechanisms responsible in this evasion are not clear. Several groups have demonstrated weak or absent HCV‐specific CD4+ T cell responses during chronic HCV infection using proliferation assays and, more recently, class II tetramers.

Julie Polson, William M. Lee – 19 April 2005

Jay H. Hoofnagle – 19 April 2005

Neil Kaplowitz – 19 April 2005

Suthat Liangpunsakul, Dhanashri Kolwankar, Amar Pinto, J. Christopher Gorski, Stephen D. Hall, Naga Chalasani – 19 April 2005 – Alcohol consumption is known to induce hepatic CYP2E1 activity, but its effect on hepatic and intestinal CYP3A in humans is not known. We have conducted a study to compare the CYP2E1 and CYP3A activities in 20 individuals with moderate alcohol consumption and 20 gender‐, race‐. and body mass index (BMI)‐matched nonalcoholics.

Roong Zhao, Stephen A. Duncan – 19 April 2005

Scott Biggins, Norah Terrault – 19 April 2005

Gianfranco Alpini, Shannon Glaser, Leonardo Baiocchi, Heather Francis, Xuefeng Xia, Gene LeSage – 19 April 2005 – The role of the cholangiocyte apical Na+‐dependent bile acid transporter (ASBT) in bile formation is unknown. Bile acid absorption by bile ducts results in cholehepatic shunting, a pathway that amplifies the canalicular osmotic effects of bile acids. We tested in isolated cholangiocytes if secretin enhances ASBT translocation to the apical membrane from latent preexisting intracellular stores.

Dan‐Qing Lou, Jeanne‐Claire Lesbordes, Gaël Nicolas, Lydie Viatte, Myriam Bennoun, Nico Van Rooijen, Axel Kahn, Laurent Renia, Sophie Vaulont – 19 April 2005 – Hepcidin, a recently discovered iron regulatory peptide, is believed to inhibit the release of iron from absorptive enterocytes and macrophages. Liver hepcidin synthesis is induced in vivo by iron stores and inflammation. The molecular basis of the regulation of hepcidin gene expression by these effectors in hepatocytes is currently unknown, although there is strong evidence that indirect mechanisms are involved.

Luigi E. Adinolfi, Diego Ingrosso, Giuseppe Cesaro, Amelia Cimmino, Maria D'Antò, Rosanna Capasso, Vincenzo Zappia, Giuseppe Ruggiero – 19 April 2005 – The factors and mechanisms implicated in the development of hepatitis C virus (HCV)‐related steatosis are unknown. Hyperhomocysteinemia causes steatosis, and the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism induces hyperhomocysteinemia. We investigated the role of these factors in the development of HCV‐related steatosis and in the progression of chronic hepatitis C (CHC).