1. Hepatitis C virus infects T cells and affects interferon-γ signaling in T cell lines
- Author
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Kondo, Yasuteru, Sung, Vicky M.H., Machida, Keigo, Liu, Minyi, and Lai, Michael M.C.
- Subjects
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HEPATITIS C , *LYMPHOCYTES , *T cells , *VIRAL proteins - Abstract
Abstract: 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-γ signaling. Indeed, T-bet and STAT-1 mRNA levels after interferon-γ 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-γ/STAT-1/T-bet signaling due to the reduction of STAT-1 and inhibition of its activation (phosphorylation). [Copyright &y& Elsevier]
- Published
- 2007
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