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SEN virus: Response to interferon alfa and influence on the severity and treatment response of coexistent hepatitis C
Author(s) -
Umemura Takeji,
Alter Harvey J.,
Tanaka Eiji,
Orii Koji,
Yeo Anthony E. T.,
Shih J. WaiKuo,
Matsumoto Akihiro,
Yoshizawa Kaname,
Kiyosawa Kendo
Publication year - 2002
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1053/jhep.2002.32536
Subject(s) - medicine , hepatitis c virus , hepatitis , interferon , alpha interferon , interferon alfa , hepatitis c , immunology , virus , virology , hepacivirus , flaviviridae
The SEN virus (SENV) is a recently identified single‐stranded, circular DNA virus. A strong association between 2 SENV variants (SENV‐D and SENV‐H) and transfusion‐associated non–A‐to‐E hepatitis has been reported. To clarify the effect of SENV infection on coexisting chronic hepatitis C and the effect of interferon alfa (IFN‐α) therapy on SENV replication, SENV DNA was quantitated by polymerase chain reaction in serum samples from 186 patients with chronic hepatitis C. Thirty‐nine of 186 (21%) patients with chronic hepatitis C were positive for SENV DNA. There were no differences in the clinical, virologic and histologic features between patients with and without SENV infection. Eighteen of 102 patients with chronic hepatitis C who received IFN‐α were positive for SENV DNA. The sustained response rate for hepatitis C virus (HCV) clearance after IFN‐α treatment did not differ significantly between patients with SENV (28%) and without SENV infection (39%). SENV DNA levels decreased during therapy in 15 of 16 patients, and 11 of the 16 patients (69%) had a sustained loss of SENV DNA in response to IFN‐α. In coinfected patients, SENV responses to IFN‐α were significantly better in those who failed to clear HCV RNA than in those who lost HCV RNA ( P = .013). In conclusion, SENV infection was frequently found in patients with chronic hepatitis C. SENV infection had no apparent influence on the severity of HCV‐related liver disease or the HCV response to IFN‐α. SENV was sensitive to IFN‐α therapy and the majority of patients had a sustained virologic response.