Nguyen Linh Toan
Nguyen Linh Toan, Vietnam Military Medical University, Vietnam
Nguyen L Toan recieved his medical doctor degree from Hanoi Medical University, Vietnam and Ph.D. from University of Tuebingen, Germany. Currently, he is an Associate Professor of Pathophysiology and Chief of Department of Pathophysiology, Vietnam Military Medical University. He has published more than 17 papers in international peer-review science journals.
Hepatitis B caused by hepatitis B virus (HBV) infection is the major infectious disease with more than 350 million chronic carriers and approximately 1.2 million people die of HBV infection causes annually worldwide. HBV infection and HBV-related liver diseases are one of the most major health problems in Vietnam. Infection with different genotypes and mixtures of genotypes of HBV significantly affects the pathogenesis and clinical outcomes of HBV infection. Interplay between HBV infection and host immune response leads to a large spectrum of pathologies including acute and chronic hepatitis progressing to liver cirrhosis and hepatocellular carcinoma (HCC). Host genetic polymorphisms in various genes including Interferon alpha (IFN-alpha2), interferon-alpha receptor-1 (IFNAR1), complement genes (MBL and FCN2), MICA, CISH and STAT4 are significantly associated with susceptibility to HBV infection and progression of disease in Vietnamese population. Particularly, the deletion in the promoter region of IFN-alpha2 gene, two variants in interferon-alpha receptor-1gene(IFNAR1), variant at codon 54 of MBL and the haplotypes based on 4 functional variants of FCN2 gene, are significantly associated with clinical outcomes and subsequent disease progression. The MICA promoter variant rs2596542 and nonsynonymous substitutions MICA-129Met/Val, MICA-251Gln/Arg, MICA-175Gly/Ser, triplet repeat polymorphism and respective haplotypes are significantly contributed to HBV-induced HCC and HBV persistence. In addition, soluble serum levels of ficolin-2, MICA protein that modulated by gene variation influence the course and clinical progression of HBV infection. We conclude that molecular interaction between virus and host genetic variation play a central role during HBV infection and disease progression.
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