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Journal of Clinical Microbiology, September 2002, p. 3140-3145, Vol. 40, No. 9
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.9.3140-3145.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Weak Association between SEN Virus Viremia and Liver Disease

Hideo Yoshida,* Naoya Kato, Yasushi Shiratori, Runxuan Shao, Yue Wang, Shuichiro Shiina, and Masao Omata

Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan

Received 22 June 2001/ Returned for modification 17 November 2001/ Accepted 13 June 2002

Recently, a novel DNA virus designated SEN virus (SEN-V), which is thought to be related to posttransfusion hepatitis, was discovered. The aim of the present study was to clarify the relationship between SEN-V infection and the development of liver disease. We examined SEN-V from the sera of 21 patients with non-B, non-C hepatocellular carcinoma (HCC) and 13 patients with non-B, non-C chronic liver disease (CLD) without HCC who were admitted to our hospital between 1995 and 1997. Thirty-two patients without liver disease served as controls and were also examined for SEN-V. SEN-V DNA was detected by the nested PCR method after extraction of DNA from serum. SEN-V DNA was detected in 74% (25 of 34) of patients with CLD with or without HCC who were negative for both hepatitis B virus surface antigen and anti-hepatitis C virus antibody. SEN-V DNA was detected in 69% (9 of 13) of CLD patients without HCC and in 76% (16 of 21) of HCC patients. The prevalence of SEN-V was no higher in patients with liver disease than in patients without liver disease (24 of 32; 75%). There were no significant differences in age, sex, liver function, history of blood transfusion, or amount of alcohol intake between SEN-V-positive and SEN-V-negative CLD and HCC patients. Genetic analysis suggested that SEN-V is closely related to the TT virus family. SEN-V was detected at almost the same frequency in patients with and without liver disease. SEN-V does not seem to contribute either to the pathogenesis of liver disease or to the development of HCC from chronic liver disease.

* Corresponding author. Mailing address: Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Phone: 81-3-3815-5411, ext. 33056. Fax: 81-3-3814-0021. E-mail: ch2h-ysd{at}asahi-net.or.jp.

Journal of Clinical Microbiology, September 2002, p. 3140-3145, Vol. 40, No. 9
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.9.3140-3145.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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