EXPERIMENTAL AND MOLECULAR PATHOLOGY, cilt.96, sa.1, ss.36-41, 2014 (SCI-Expanded)
Background: The Jak-STAT signaling of hepatitis C virus (HCV) infected hepatocyte is critical for the antiviral action of endogenously produced interferon (IFN) as well as exogenously administered interferon alpha (IFN-a). The activation of cellular Jak-STAT signaling by IFN-alpha results in the phosphorylation and nuclear translocation of pSTAT1 and pSTAT2 proteins to induce antiviral gene transcription. Clinical studies show that chronic HCV patients with high viral load show poor response to interferon alpha and ribavirin combination therapy.