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Distinct subpopulations of hepatitis C virus infectious cells with different levels of intracellular hepatitis C virus core protein
Author(s) -
Wang ShuChi,
Yang JengFu,
Wang ChaoLing,
Huang ChungFeng,
Lin YuYin,
Chen YiYou,
Lo ChungTing,
Lee PoYen,
Wu KuanTa,
Lin ChiaI.,
Hsieh MengHsuan,
Chuang HungYi,
Ho ChiKung,
Yu MingLung,
Dai ChiaYen
Publication year - 2016
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1016/j.kjms.2016.08.002
Subject(s) - hepatocellular carcinoma , medicine , hepatitis c virus , virus , virology , carcinogenesis , viral load , gene , viral hepatitis , polymerase chain reaction , dna damage , hepatitis b virus , gene expression , immunology , dna , biology , cancer , cancer research , genetics
Chronic infection by hepatitis C virus (HCV) is a major risk factor for the development of hepatocellular carcinoma (HCC). Despite the clear clinical importance of virus‐associated HCC, the underlying molecular mechanisms remain largely unclarified. Oxidative stress, in particular, DNA lesions associated with oxidative damage, plays a major role in carcinogenesis, and is strongly linked to the development of many cancers, including HCC. However, in identifying hepatocytes with HCV viral RNA, estimates of the median proportion of HCV‐infected hepatocytes have been found as high as 40% in patients with chronic HCV infection. In order to explore the gene alternation and association between different viral loads of HCV‐infected cells, we established a method to dissect high and low viral load cells and examined the expression of DNA damage‐related genes using a quantitative polymerase chain reaction array. We found distinct expression patterns of DNA damage‐related genes between high and low viral load cells. This study provides a new method for future study on virus‐associated gene expression research.

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