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A novel mechanism in which HCV infection activates STAT3 through multiple cellular signaling pathways. During HCV infection, the viral protein NS4B activates the expression of several members of the PKC family, stimulates the JNK/ERK signaling cascade, represses the SOCS3 expression, and enhances STAT3 activity, which in turn stimulates MMP-2 and Bcl-2 expression, resulting in the control of cell transformation, apoptosis, and tumorigenesis in response to HCV infection.
