AIM: To clarify the effect of SEN virus (SENV) infection on a combination therapy including interferon alfa (IFN-alpha) or pegylated-IFN with ribavirin in patients with chronic hepatitis and the effect of a combination therapy on SENV. METHODS: SENV DNA was determined by polymerase chain reaction in serum samples from 95 patients with chronic hepatitis C. Quantitative analysis was done for SENV H DNA. RESULTS: Twenty-one (22%) of 95 patients were positive for SENV DNA. There was no difference in clinical and biochemical parameters between patients with HCV infection alone and coinfected patients. The sustained response rate for HCV clearance after combination therapy did not differ between patients with SENV (52%) and without SENV (50%, n.s.). SENV DNA was undetectable in 76% of the initially SENV positive patients at the end of follow-up. SENV H response to combination therapy was significantly correlated with SENV DNA level (P=0.05). CONCLUSION: SENV infection had no influence on the HCV sustained response rate to the combination therapy. Response rate of SENV to the combination therapy depends on SENV DNA level.
AIM: To clarify the effect of SEN virus (SENV) infection on a combination therapy including interferon alfa (IFN-alpha) or pegylated-IFN with ribavirin in patients with chronic hepatitis and the effect of a combination therapy on SENV. METHODS:SENV DNA was determined by polymerase chain reaction in serum samples from 95 patients with chronic hepatitis C. Quantitative analysis was done for SENV H DNA. RESULTS: Twenty-one (22%) of 95 patients were positive for SENV DNA. There was no difference in clinical and biochemical parameters between patients with HCV infection alone and coinfectedpatients. The sustained response rate for HCV clearance after combination therapy did not differ between patients with SENV (52%) and without SENV (50%, n.s.). SENV DNA was undetectable in 76% of the initially SENV positive patients at the end of follow-up. SENV H response to combination therapy was significantly correlated with SENV DNA level (P=0.05). CONCLUSION:SENVinfection had no influence on the HCV sustained response rate to the combination therapy. Response rate of SENV to the combination therapy depends on SENV DNA level.
Authors: A L Zignego; R Fontana; S Puliti; S Barbagli; M Monti; G Careccia; F Giannelli; C Giannini; G Buzzelli; M R Brunetto; F Bonino; P Gentilini Journal: Arch Virol Date: 1997 Impact factor: 2.574
Authors: Y Nishizawa; E Tanaka; K Orii; A Rokuhara; T Ichijo; K Yoshizawa; K Kiyosawa Journal: J Gastroenterol Hepatol Date: 2000-11 Impact factor: 4.029
Authors: M P Manns; J G McHutchison; S C Gordon; V K Rustgi; M Shiffman; R Reindollar; Z D Goodman; K Koury; M Ling; J K Albrecht Journal: Lancet Date: 2001-09-22 Impact factor: 79.321
Authors: T Umemura; A E Yeo; A Sottini; D Moratto; Y Tanaka; R Y Wang; J W Shih; P Donahue; D Primi; H J Alter Journal: Hepatology Date: 2001-05 Impact factor: 17.425
Authors: T Poynard; P Marcellin; S S Lee; C Niederau; G S Minuk; G Ideo; V Bain; J Heathcote; S Zeuzem; C Trepo; J Albrecht Journal: Lancet Date: 1998-10-31 Impact factor: 79.321
Authors: Elmoeiz A Elnagi; Thekra N Al-Maqati; Yaser Alnaam; Ahmed A Adam; Ali A Rabaan; Zeinab S Mohamed; Anisah Amer; Hussa L Almarfoi Journal: Saudi J Biol Sci Date: 2021-04-01 Impact factor: 4.219