https://scholars.lib.ntu.edu.tw/handle/123456789/627779
標題: | Hepatitis C virus infects T cells and affects interferon-gamma signaling in T cell lines | 作者: | Kondo, Yasuteru Sung, Vicky M H Machida, Keigo HELENE MINYI LIU Lai, Michael M C |
關鍵字: | CD4; CD45RA; STAT-1; T-bet; lymphotropism; HCV; POLYMERASE-CHAIN-REACTION; BLOOD MONONUCLEAR-CELLS; IN-VITRO; LIVER INFLAMMATION; IMMUNE-RESPONSES; RNA REPLICATION; HCV; EXPRESSION; CD81; LYMPHOCYTES | 公開日期: | 25-四月-2007 | 出版社: | ACADEMIC PRESS INC ELSEVIER SCIENCE | 卷: | 361 | 期: | 1 | 起(迄)頁: | 161 | 來源出版物: | Virology | 摘要: | It has been reported that hepatitis C virus (HCV) may infect and replicate in human T cells, particularly in perihepatic lymph nodes, but the extent and consequence of T-cell infection in patients is unclear. This study is conducted to characterize the parameters and functional consequences of HCV infection in T lymphocytes. By using a lymphotropic HCV strain, we showed that HCV could infect T cell lines (Molt-4 and Jurkat cells) in vitro. Both positive- and negative-strand HCV RNA were detected for several weeks after infection. Viral proteins could also be detected by immunofluorescence studies. Moreover, infectious HCV particles were produced from Molt-4 cell cultures, and could be used to infect naïve T cell lines. HCV could also infect human primary CD4+ T cells, particularly naïve (CD45RA+CD45RO-) CD4+ cells, in culture. The amounts of STAT-1 and phosphorylated STAT-1 proteins in the infected Molt-4 cells were significantly less than those in uninfected cultures, suggesting the possibility of defect in interferon-gamma signaling. Indeed, T-bet and STAT-1 mRNA levels after interferon-gamma stimulation in infected Molt-4 were suppressed. In conclusion, HCV could infect and transiently replicate in T cells and that HCV replication suppressed the IFN-gamma/STAT-1/T-bet signaling due to the reduction of STAT-1 and inhibition of its activation (phosphorylation). |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/627779 | ISSN: | 0042-6822 | DOI: | 10.1016/j.virol.2006.11.009 |
顯示於: | 生物化學暨分子生物學科研究所 |
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