As such, NR-targeted treatment strategies will add to the evolving field of individualized medicine in hepatology. Future drug development should take advantage of the fascinating explosion of new relevant ERK inhibitor and unexpected information that place NR pathways into the heart of liver function in health and disease. Over the next years we may also hope to obtain further insights into the role of genetic NR variants as modifiers of liver disease and additional NR-based therapeutics, expanding our armamentarium to combat both common and orphan liver diseases. Note: The tables and associated text are available as Supporting Material

1. Only the first seven references in the introduction section of this article are available below in print. The remaining

references are available online only with the electronic version of this article as Supporting Material 2. To access the remaining references, visit the online version of Hepatology at http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1527-3350. this website Additional supporting information may be found in the online version of this article. “
“Human immunodeficiency virus (HIV) co-infection accelerates both hepatitis C (HCV) and hepatitis B (HBV) natural history leading to faster progression to and increased incidence of cirrhosis, hepatocellular carcinoma (HCC) and death. HIV/HCV co-infected patients have twice the risk of developing cirrhosis and a sixfold increased risk of liver failure compared with those with HCV alone. Effective treatment of HBV and HCV in HIV co-infected patients increases survival. Treatment responses to TVR do not differ between HIV/HCV co-infected and HCV mono-infected patients. In patients treated with TVR combination treatment, overall safety and tolerability profile was comparable to that previously observed in chronic genotype 1 HCV mono-infected patients. In HIV/HBV co-infected patients, any treatment decision for hepatitis B should take into account the possible impact on HIV and vice-versa. For HIV/HBV co-infected patients, initiation of ART with active anti-HBV coverage is now recommended at any CD4+ T-cell count to reduce the risk of liver disease

progression. “
“Background MCE and Aim:  We intended to investigate the effects of pre-existing mutations at reverse transcriptase region of hepatitis B virus (HBV) on the occurrence of virological breakthrough (VB) to adefovir dipivoxil (ADV) in patients with lamivudine (LAM)-resistant chronic hepatitis B (CHB). Methods:  Ninety-seven patients with LAM-resistant CHB were treated with ADV at a dose of 10 mg daily, and were followed for a median period of 13 months. Just before the initiation of ADV therapy, the whole length of reverse transcriptase region of serum HBV-DNA was sequenced using direct sequencing. Results:  All patients had genotype C HBV and mutations in the YMDD motif, specifically, YIDD (65%), YVDD (28%), or both (7%).