Hepatitis C virus core protein inhibits interleukin 12 and nitric oxide production from activated macrophages

Chu Hee Lee, Yo Han Choi, Se Hwan Yang, Chang Woo Lee, Sang Jun Ha, Young Chul Sung

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67 Citations (Scopus)

Abstract

A characteristic feature of hepatitis C virus (HCV) infection is a high frequency of persistence and the progression to chronic liver diseases. Recent data suggest that prevalent T helper (Th) 2 immunity as well as weak HCV-specific T-cell response is associated with viral persistence. Here, we showed that the production of interleukin 12 (IL-12) and nitric oxide (NO) that is critical for the induction of Th1 and innate immunity, but not that of tumor necrosis factor α (TNF-α), was significantly suppressed in both HCV core-expressing macrophage cell lines and mouse peritoneal macrophages treated with recombinant core protein. In addition, IL-12 p40 promoter activity was repressed by the presence of HCV core in macrophages stimulated with lipopolysaccharride (LPS) following IFN-γ treatment, indicating that IL-12 production may be downregulated at the transcriptional level. We also found that proliferation of T cells and IFN-γ, production in mixed lymphocyte reactions (MLR) with core-expressing cells were inhibited. Taken together, our results suggest that HCV core protein could play roles in suppressing the induction of Th1 immunity through inhibition of IL-12 and NO production.

Original languageEnglish
Pages (from-to)271-279
Number of pages9
JournalVirology
Volume279
Issue number1
DOIs
Publication statusPublished - 2001 Jan 20

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All Science Journal Classification (ASJC) codes

  • Virology

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