Hepatitis B virus X protein: TRIMming antiviral defences in hepatocytes

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In Silico Prediction and Docking of Tertiary Structure of Multifunctional Protein X of Hepatitis B Virus

Hepatitis B virus (HBV) infection is a universal health problem and may result into acute, fulminant, chronic hepatitis liver cirrhosis, or hepatocellular carcinoma. Sequence for protein X of HBV was retrieved from Uniprot database. ProtParam from ExPAsy server was used to investigate the physicochemical properties of the protein. Homology modeling was carried out using Phyre2 server, and refin...

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The hepatitis B virus X protein disrupts innate immunity by downregulating mitochondrial antiviral signaling protein.

Previous studies have shown that both hepatitis A virus and hepatitis C virus inhibit innate immunity by cleaving the mitochondrial antiviral signaling (MAVS) protein, an essential component of the virus-activated signaling pathway that activates NF-kappaB and IFN regulatory factor-3 to induce the production of type I IFN. For human hepatitis B virus (HBV), hepatitis B s-Ag, hepatitis B e-Ag, o...

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Hepatitis B Virus X Protein and Hepatocarcinogenesis

Chronic hepatitis B virus (HBV) infection is one of the most associated factors in hepatocarcinogenesis. HBV is able to integrate into the host genome and encode the multi-functional hepatitis B virus x protein (HBx). Although the mechanism between HBx and carcinogenesis is still elusive, recent studies have shown that HBx was able to influence various signaling pathways, as well as epigenetic ...

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Expression of Hepatitis B Virus X Protein in Hepatocytes Suppresses CD8+ T Cell Activity

BACKGROUND CD8(+) T cells contribute to the clearance of Hepatitis B virus (HBV) infection and an insufficient CD8(+) T cell response may be one of the major factors leading to chronic HBV infection. Since the HBx antigen of HBV can up-regulate cellular expression of several immunomodulatory molecules, we hypothesized that HBx expression in hepatocytes might affect CD8(+) T cell activity. MET...

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ژورنال

عنوان ژورنال: Gut

سال: 2017

ISSN: 0017-5749,1468-3288

DOI: 10.1136/gutjnl-2017-314013