The RNA genome of hepatitis E virus robustly triggers an antiviral interferon response

Wenshi Wang, Yijin Wang, Changbo Qu, Shan Wang, Jianhua Zhou, Wanlu Cao, Lei Xu, Buyun Ma, Mohamad S. Hakim, Yuebang Yin, Tiancheng Li, Maikel P. Peppelenbosch, Jingmin Zhao, Qiuwei Pan – 1 December 2017 – The outcomes of hepatitis E virus (HEV) infection are diverse, ranging from asymptomatic carrier, self‐limiting acute infection, and fulminant hepatitis to persistent infection. This is closely associated with the immunological status of the host. This study aimed to understand the innate cellular immunity as the first‐line defense mechanism in response to HEV infection.

Standardized hybrid living donor hemihepatectomy in adult‐to‐adult living donor liver transplantation

Susumu Eguchi, Akihiko Soyama, Takanobu Hara, Koji Natsuda, Satomi Okada, Takashi Hamada, Taiichiro Kosaka, Shinichiro Ono, Tomohiko Adachi, Masaaki Hidaka, Mitsuhisa Takatsuki – 1 December 2017 – The aim of this study was to analyze the outcomes of the most updated version and largest group of our standardized hybrid (laparoscopic mobilization and hepatectomy through midline incision) living donor (LD) hemihepatectomy compared with those from a conventional laparotomy in adult‐to‐adult living donor liver transplantation (LDLT).

New insights into the role and mechanism of c‐Jun‐N‐terminal kinase signaling in the pathobiology of liver diseases

Sanda Win, Tin Aung Than, Jun Zhang, Christina Oo, Robert Win Maw Min, Neil Kaplowitz – 30 November 2017 – The c‐Jun‐N‐terminal‐kinase (JNK) family is highly conserved across species such as Drosophila, C. elegans, zebrafish and mammals, and plays a central role in hepatic physiologic and pathophysiologic responses. These responses range from cell death to cell proliferation and carcinogenesis, as well as metabolism and survival, depending on the specific context and duration of activation of the JNK signaling pathway.

Global microRNA expression profiling in the liver biopsies of hepatitis B virus–infected patients suggests specific microRNA signatures for viral persistence and hepatocellular injury

Avishek Kumar Singh, Sheetalnath Babasaheb Rooge, Aditi Varshney, Madavan Vasudevan, Ankit Bhardwaj, Senthil Kumar Venugopal, Nirupama Trehanpati, Manoj Kumar, Robert Geffers, Vijay Kumar, Shiv Kumar Sarin – 30 November 2017 – Hepatitis B virus (HBV) can manipulate the microRNA (miRNA) regulatory networks in infected cells to create a permissive environment for viral replication, cellular injury, disease onset, and its progression.

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