Hepatitis C virus infects T cells and affects interferon-γ signaling in T cell lines

Yasuteru Kondo, Vicky M.H. Sung, Keigo Machida, Minyi Liu, Michael M.C. Lai

Research output: Contribution to journalArticlepeer-review

60 Citations (Scopus)


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).

Original languageEnglish
Pages (from-to)161-173
Number of pages13
Issue number1
Publication statusPublished - 2007 Apr 25
Externally publishedYes


  • CD4
  • CD45RA
  • HCV
  • Lymphotropism
  • STAT-1
  • T-bet

ASJC Scopus subject areas

  • Virology


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