Background: Interferon (IFN)-α/β exerts its antiproliferative and immunoregulatory activities via specific cell surface receptors, the interferon c/I3 receptors (IFNABR). Expression of IFNABR genes was found to be significantly higher in hepatic tissue of chronic hepatitis C patients than in normal and cirrhotic livers. Soluble form IFN receptors present in serum were implied in counteracting IFN responses when treating chronic hepatitis C. Methods: Peripheral blood specimens were collected from 24 normal controls and 76 chronic hepatitis C patients receiving IFN-ribavirin combined therapy. After RNA isolation, expression of IFNABR genes was assessed by semi-quantitative RT-PCR. Pretreatment serum ALT level, genotype and serum concentration of HCV were determined and correlated to IFNABR gene expression. Results: A significantly lower expression of IFNABR gene was found in peripheral blood cells of patients with hepatitis C as compared to that in control individuals (P<0.0001). When patients were further classified according to their previous exposure to IFN treatment, the difference of IFNABR gene expression level was statistically significant both in naïve (P=0.0025, N=46) and in relapsed (P=0.013, N=30) patients. In the patient group, 23 of them received a complete course of IFN-ribavirin therapy, and were followed up for more than 6 months. Expression level of IFNABR gene was found to be lower in the sustained responders than non-responders (P=0.077). Serum ALT concentration was not found to correlate with IFNABR gene expression. Conclusion: To our knowledge, this is the first report trying to correlate the expression of IFN receptor genes in the peripheral blood cells with other factors related to the responsiveness to IFN therapy in chronic hepatitis C. Based on our preliminary results, the long-term response toward IFN therapy in chronic hepatitis C patients might be easily predicted by the expression level of IFNABR in peripheral blood cells.
Background: Interferon (IFN)-α/β exerts its antiproliferative and immunoregulatory activities via specific cell surface receptors, the interferon c/I3 receptors (IFNABR). Expression of IFNABR genes was found to be significantly higher in hepatic tissue of chronic hepatitis C patients than in normal and cirrhotic livers. Soluble form IFN receptors present in serum were implied in counteracting IFN responses when treating chronic hepatitis C. Methods: Peripheral blood specimens were collected from 24 normal controls and 76 chronic hepatitis C patients receiving IFN-ribavirin combined therapy. After RNA isolation, expression of IFNABR genes was assessed by semi-quantitative RT-PCR. Pretreatment serum ALT level, genotype and serum concentration of HCV were determined and correlated to IFNABR gene expression. Results: A significantly lower expression of IFNABR gene was found in peripheral blood cells of patients with hepatitis C as compared to that in control individuals (P<0.0001). When patients were further classified according to their previous exposure to IFN treatment, the difference of IFNABR gene expression level was statistically significant both in naïve (P=0.0025, N=46) and in relapsed (P=0.013, N=30) patients. In the patient group, 23 of them received a complete course of IFN-ribavirin therapy, and were followed up for more than 6 months. Expression level of IFNABR gene was found to be lower in the sustained responders than non-responders (P=0.077). Serum ALT concentration was not found to correlate with IFNABR gene expression. Conclusion: To our knowledge, this is the first report trying to correlate the expression of IFN receptor genes in the peripheral blood cells with other factors related to the responsiveness to IFN therapy in chronic hepatitis C. Based on our preliminary results, the long-term response toward IFN therapy in chronic hepatitis C patients might be easily predicted by the expression level of IFNABR in peripheral blood cells.