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Decreased phorbol myristate acetate-induced release of tumor necrosis factor-alpha and interleukin-1 beta from peripheral blood monocytes of patients chronically infected with hepatitis C virus.

Hepatitis C virus (HCV) has been detected in peripheral blood mononuclear cells (PBMC) from persons chronically infected with HCV. Reports describe altered monocytic function during HCV infection; however, the immunologic consequences of HCV tropism for human macrophages are not well defined. Thus, the possibility that HCV infection of monocytes may alter patterns of cytokine release was investigated. The in vitro secretion of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta in response to phorbol myristate acetate-stimulated monocytes and PBMC of subjects chronically infected or not infected with HCV was compared. TNF-alpha and IL-1 beta release were suppressed in cells from infected subjects. Although virus-induced immunosuppression is not a major clinical syndrome of HCV infection, the findings support a hypothesis that HCV can induce selective defects in antigen-presenting cells that may enhance the ability of HCV to persist despite the presence of cytotoxic killer cells and antibody directed against HCV.