The antiviral drug selected hepatitis B virus rtA181T/sW172* mutant has a dominant negative secretion defect and alters the typical profile of viral rebound

Nadia Warner, Stephen Locarnini – 20 June 2008 – The hepatitis B virus (HBV) mutation that encodes rtA181T is selected in the viral polymerase during antiviral drug therapy and can also encode a stop codon in the overlapping surface gene at amino acid 172 (sW172*) resulting in truncation of the last 55 amino acids of the C‐terminal hydrophobic region of the surface proteins. This mutation is usually detected as a mixed population with wild‐type HBV.

Retinol‐binding protein 4: A new marker of virus‐induced steatosis in patients infected with hepatitis c virus genotype 1

Salvatore Petta, Calogero Cammà, Vito Di Marco, Nicola Alessi, Francesco Barbaria, Daniela Cabibi, Rosalia Caldarella, Stefania Ciminnisi, Anna Licata, Maria Fatima Massenti, Alessandra Mazzola, Giuseppe Tarantino, Giulio Marchesini, Antonio Craxì – 20 June 2008 – Retinol‐binding protein 4 (RBP4) is an adipocytokine associated with insulin resistance (IR). We tested serum levels of RBP4 to assess its link with steatosis in patients with genotype 1 chronic hepatitis C (CHC) or nonalcoholic fatty liver disease (NAFLD).

Risk of severe liver disease in nonalcoholic fatty liver disease with normal aminotransferase levels: A role for insulin resistance and diabetes

Anna Ludovica Fracanzani, Luca Valenti, Elisabetta Bugianesi, Marco Andreoletti, Agostino Colli, Ester Vanni, Cristina Bertelli, Erika Fatta, Daniela Bignamini, Giulio Marchesini, Silvia Fargion – 30 May 2008 – It is uncertain whether patients with nonalcoholic fatty liver disease (NAFLD) and normal alanine aminotransferase (ALT) have a milder disease and should undergo liver biopsy.

The genetic background modulates susceptibility to mouse liver Mallory‐Denk body formation and liver injury

Shinichiro Hanada, Pavel Strnad, Elizabeth M. Brunt, M. Bishr Omary – 30 May 2008 – Mallory‐Denk bodies (MDBs) are hepatocyte inclusions found in several liver diseases and consist primarily of keratins 8 and 18 (K8/K18) and ubiquitin that are cross‐linked by transglutaminase‐2. We hypothesized that genetic variables contribute to the extent of MDB formation, because not all patients with an MDB‐associated liver disease develop inclusions.

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