Antiviral resistance and hepatitis B therapy

Marc G. Ghany, Edward C. Doo – 27 April 2009 – The management of chronic hepatitis B currently rests with long‐term therapy using oral nucleoside analogs. The major limitation of long‐term therapy is antiviral resistance. Antiviral resistance is due to the high rate of mutations that can occur during hepatitis B virus (HBV) replication and the selection of these mutants due to a replication advantage in the presence of the antiviral agent. Indeed, high rates of antiviral resistance have been found with long‐term use of lamivudine, in up to 76% of patients treated for 5 years or more.

The cyclophilin inhibitor Debio 025 combined with PEG IFNα2a significantly reduces viral load in treatment‐naïve hepatitis C patients

Robert Flisiak, Saya V. Feinman, Maciej Jablkowski, Andrzej Horban, Wieslaw Kryczka, Małgorzata Pawlowska, Jenny E. Heathcote, Giuseppe Mazzella, Carmen Vandelli, Valérie Nicolas‐Métral, Pierre Grosgurin, Jorge S.

Hepatitis B virus X protein enhances the transcriptional activity of the androgen receptor through c‐Src and glycogen synthase kinase‐3β kinase pathways

Wan‐Jen Yang, Ching‐Ju Chang, Shiou‐Hwei Yeh, Wei‐Hsiang Lin, Sheng‐Han Wang, Ting‐Fen Tsai, Ding‐Shinn Chen, Pei‐Jer Chen – 27 April 2009 – Hepatitis B virus (HBV)‐related hepatocellular carcinoma (HCC) occurs predominantly in men. By enhancing the transcriptional activity of the androgen receptor (AR) gene in a ligand‐dependent manner, the HBV X protein (HBx) might contribute to this disparity between sexes. To dissect the mechanisms underlying HBx‐enhanced AR transactivation, we investigated the effect of HBx on two critical steps in the regulation of ligand‐stimulated AR activities.

Diverse roles of invariant natural killer T cells in liver injury and fibrosis induced by carbon tetrachloride

Ogyi Park, Won‐IL Jeong, Lei Wang, Hua Wang, Zhe‐Xiong Lian, M. Eric Gershwin, Bin Gao – 27 April 2009 – Liver fibrosis is a common scarring response to all forms of chronic liver injury and is always associated with inflammation that contributes to fibrogenesis. Although a variety of cell populations infiltrate the liver during inflammation, it is generically clear that CD8 T lymphocytes promote while natural killer (NK) cells inhibit liver fibrosis. However, the role of invariant natural killer T (iNKT) cells, which are abundant in the liver, in hepatic fibrogenesis, remains obscure.

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