Interferon alpha induced intrahepatic pSTAT1 inversely correlate with serum HCV RNA levels in chronic HCV infection

Gunduz F., Mallikarjun C., Balart L. A., Dash S.

EXPERIMENTAL AND MOLECULAR PATHOLOGY, cilt.96, sa.1, ss.36-41, 2014 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 96 Sayı: 1
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1016/j.yexmp.2013.10.016
  • Dergi Adı: EXPERIMENTAL AND MOLECULAR PATHOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.36-41
  • Marmara Üniversitesi Adresli: Evet

Özet

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.