Assembly and budding of a hepatitis B virus is mediated by a novel type of intracellular vesicles

Mouna Mhamdi, Anneke Funk, Heinz Hohenberg, Hans Will, Hüseyin Sirma – 13 June 2007 – Formation of enveloped viruses involves assembly and budding at cellular membranes. In this study, we elucidated the morphogenesis of hepadnaviruses on the ultrastructural and biochemical level using duck hepatitis B virus (DHBV) as a model system. Formation of virus progeny initiates at the endoplasmic reticulum (ER) and is conserved both in vitro and in vivo.

FIB‐4: An inexpensive and accurate marker of fibrosis in HCV infection. comparison with liver biopsy and fibrotest

Anaïs Vallet‐Pichard, Vincent Mallet, Bertrand Nalpas, Virginie Verkarre, Antoine Nalpas, Valérie Dhalluin‐Venier, Hélène Fontaine, Stanislas Pol – 13 June 2007 – To optimize the management of patients with chronic hepatitis C virus (HCV) infection, noninvasive tests to determine the degree of hepatic fibrosis have been developed.

Predictors of response of U.S. veterans to treatment for the hepatitis C virus

Lisa I. Backus, Derek B. Boothroyd, Barbara R. Phillips, Larry A. Mole – 13 June 2007 – The currently recommended treatment for hepatitis C virus (HCV) infection is pegylated interferon alfa (PEG‐INF) and ribavirin, which can be difficult to tolerate. More information about predicting sustained virologic response (SVR) may allow more informed treatment decisions to be made. This retrospective observational cohort study identified predictors of SVR to PEG‐INF and ribavirin in routine medical practice at 121 Department of Veterans Affairs facilities.

Hepatitis C virus protein expression causes calcium‐mediated mitochondrial bioenergetic dysfunction and nitro‐oxidative stress

Claudia Piccoli, Rosella Scrima, Giovanni Quarato, Annamaria D'Aprile, Maria Ripoli, Lucia Lecce, Domenico Boffoli, Darius Moradpour, Nazzareno Capitanio – 13 June 2007 – Hepatitis C virus (HCV) infection induces a state of oxidative stress that is more pronounced than that in many other inflammatory diseases. In this study we used well‐characterized cell lines inducibly expressing the entire HCV open‐reading frame to investigate the impact of viral protein expression on cell bioenergetics.

Tissue‐type plasminogen activator deficiency exacerbates cholestatic liver injury in mice

Hongtao Wang, Yan Zhang, Robert O. Heuckeroth – 30 May 2007 – Recent studies demonstrating a role for plasminogen activator inhibitor (PAI)‐1 in cholestatic liver disease in mice suggested that tissue‐type plasminogen activator (tPA) or urokinase plasminogen activator (uPA) might be important after biliary tract obstruction. We now demonstrate that blocking tPA exacerbates liver injury after bile duct ligation (BDL).

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