title: SEN virus: response to interferon alfa and influence on the severity and treatment response of coexistent hepatitis C.
abstract: 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-alpha) 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-alpha were positive for SENV DNA. The sustained response rate for hepatitis C virus (HCV) clearance after IFN-alpha 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-alpha. In coinfected patients, SENV responses to IFN-alpha 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-alpha. SENV was sensitive to IFN-alpha therapy and the majority of patients had a sustained virologic response.
authors.affiliation: Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan. tumemura@mail.cc.nih.gov
authors.forename: Takeji
authors.initials: T
authors.lastname: Umemura
authors.forename: Harvey J
authors.initials: HJ
authors.lastname: Alter
authors.forename: Eiji
authors.initials: E
authors.lastname: Tanaka
authors.forename: Koji
authors.initials: K
authors.lastname: Orii
authors.forename: Anthony E t
authors.initials: AE
authors.lastname: Yeo
authors.forename: J Wai-Kuo
authors.initials: JW
authors.lastname: Shih
authors.forename: Akihiro
authors.initials: A
authors.lastname: Matsumoto
authors.forename: Kaname
authors.initials: K
authors.lastname: Yoshizawa
authors.forename: Kendo
authors.initials: K
authors.lastname: Kiyosawa
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use*; D004266:DNA Virus Infections / Q000150:complications* / Q000188:drug therapy / Q000453:epidemiology* / Q000821:virology; D004267:DNA Viruses / Q000187:drug effects; D005260:Female; D006526:Hepatitis C / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology / Q000821:virology; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D013997:Time Factors; D016896:Treatment Outcome; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D016898:Interferon-alpha