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 mononucl ear cells (PBMC) from persons chronically infected with HCV. Reports d escribe 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 ma y alter patterns of cytokine release was investigated. The in vitro se cretion of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 be ta in response to phorbol myristate acetate-stimulated monocytes and P BMC of subjects chronically infected or not infected with HCV was comp ared. TNF-alpha and IL-1 beta release were suppressed in cells from in fected subjects. Although virus-induced immunosuppression is not a maj or clinical syndrome of HCV infection, the findings support a hypothes is that HCV can induce selective defects in antigen-presenting cells t hat may enhance the ability of HCV to persist despite the presence of cytotoxic killer cells and antibody directed against HCV.