Host genetic variants influencing the clinical course of hepatitis C virus infection

被引:32
作者
Matsuura, Kentaro [1 ,2 ,3 ,4 ]
Tanaka, Yasuhito [1 ,2 ]
机构
[1] Nagoya City Univ, Grad Sch Med Sci, Dept Virol, Nagoya, Aichi, Japan
[2] Nagoya City Univ, Grad Sch Med Sci, Liver Unit, Nagoya, Aichi, Japan
[3] Nagoya City Univ, Grad Sch Med Sci, Dept Gastroenterol & Metab, Nagoya, Aichi, Japan
[4] NIH, Dept Transfus Med, Clin CenterInfect Dis & Immunogenet Sect, Bethesda, MD 20892 USA
关键词
HCV; GWAS; spontaneous clearance; fibrosis; HCC; GENOME-WIDE ASSOCIATION; SINGLE-NUCLEOTIDE POLYMORPHISMS; AMINO-ACID SUBSTITUTION; GROWTH-FACTOR GENE; HEPATOCELLULAR-CARCINOMA; SPONTANEOUS CLEARANCE; FIBROSIS PROGRESSION; FUNCTIONAL POLYMORPHISM; SPONTANEOUS RESOLUTION; PEGYLATED INTERFERON;
D O I
10.1002/jmv.24334
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The clinical course of hepatitis C virus (HCV) infection greatly differs in individuals. Various viral, host, and environmental factors influence the natural history of HCV infection. Recent genome-wide association studies identified several host genetic factors influencing treatment efficacy or clinical course in HCV infection. A landmark discovery was that IFNL3-IFNL4 variants are strongly associated with responses to interferon-based treatment. Genetic variants in IFNL3-IFNL4 as well as those in HLA class II loci influence the spontaneous clearance of acute HCV infection. Interestingly, these genetic variants also affect the activity of hepatitis, or disease progression in chronic hepatitis C. In addition, polymorphisms in apoptosis-related genes such as RNF7, TULP1, and MERTK are associated with fibrosis progression, and DEPDC5 and MICA variants are associated with HCV-related hepatocellular carcinoma. Understanding the genetic factors associated with the clinical course of HCV infection is essential for personalized treatment and surveillance of disease progression and hepatocellular carcinoma. (c) 2015 Wiley Periodicals, Inc.
引用
收藏
页码:185 / 195
页数:11
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