Toward a more complete understanding of the association between a hepatitis C sustained viral response and cause‐specific outcomes

Hamish A. Innes, Scott A. McDonald, John F. Dillon, Sam Allen, Peter C. Hayes, David Goldberg, Peter R. Mills, Stephen T. Barclay, David Wilks, Heather Valerio, Ray Fox, Diptendu Bhattacharyya, Nicholas Kennedy, Judith Morris, Andrew Fraser, Adrian J. Stanley, Peter Bramley, Sharon J. Hutchinson – 26 February 2015 – Sustained viral response (SVR) is the optimal outcome of hepatitis C virus (HCV) therapy, yet more detailed data are required to confirm its clinical value. Individuals receiving treatment in 1996‐2011 were identified using the Scottish HCV clinical database.

Adaptation of the hepatitis B virus core protein to CD8+ T‐cell selection pressure

Helenie Kefalakes, Bettina Budeus, Andreas Walker, Christoph Jochum, Gudrun Hilgard, Andreas Heinold, Falko M. Heinemann, Guido Gerken, Daniel Hoffmann, Joerg Timm – 26 February 2015 – Activation of hepatitis B virus (HBV)–specific CD8 T cells by therapeutic vaccination may promote sustained control of viral replication by clearance of covalently closed circular DNA from infected hepatocytes. However, little is known about the exact targets of the CD8 T‐cell response and whether HBV reproducibly evades CD8 T‐cell immune pressure by mutation.

Liver fibrosis occurs through dysregulation of MyD88‐dependent innate B‐cell activity

Manoj Thapa, Raghavan Chinnadurai, Victoria M. Velazquez, Dana Tedesco, Elizabeth Elrod, Jin‐Hwan Han, Prachi Sharma, Chris Ibegbu, Andrew Gewirtz, Frank Anania, Bali Pulendran, Mehul S. Suthar, Arash Grakoui – 24 February 2015 – Chronic liver disease mediated by activation of hepatic stellate cells (HSCs) leads to liver fibrosis. Here, we postulated that the immune regulatory properties of HSCs might promote the profibrogenic activity of B cells. Fibrosis is completely attenuated in carbon tetrachloride–treated, B cell–deficient µMT mice, showing that B cells are required.

A novel vascular pattern promotes metastasis of hepatocellular carcinoma in an epithelial–mesenchymal transition–independent manner

Jian‐Hong Fang, Hui‐Chao Zhou, Chong Zhang, Li‐Ru Shang, Lei Zhang, Jing Xu, Limin Zheng, Yunfei Yuan, Rong‐Ping Guo, Wei‐Hua Jia, Jing‐Ping Yun, Min‐Shan Chen, Yaojun Zhang, Shi‐Mei Zhuang – 24 February 2015 – Early metastasis is responsible for frequent relapse and high mortality of hepatocellular carcinoma (HCC), but its underlying mechanisms remain unclear. Epithelial–mesenchymal transition (EMT) has been considered a key event in metastasis.

Drug‐induced allergic hepatitis develops in mice when myeloid‐derived suppressor cells are depleted prior to halothane treatment

Mala Chakraborty, Aaron M. Fullerton, Kenrick Semple, Lynette S. Chea, William R. Proctor, Mohammed Bourdi, David E. Kleiner, Xiangbin Zeng, Pauline M. Ryan, Pradeep K. Dagur, Julia D. Berkson, Timothy P. Reilly, Lance R. Pohl – 24 February 2015 – Clinical evidence suggests that many cases of serious idiosyncratic drug‐induced liver injury are mediated by the adaptive immune system in response to hepatic drug‐protein adducts, also referred to as “drug‐induced allergic hepatitis”; but detailed mechanistic proof has remained elusive due to the lack of animal models.

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