Histopathologic impact of TT virus infection on the liver of type C chronic hepatitis and liver cirrhosis in Japan

✍ Scribed by Mitsuhiko Moriyama; Hiroshi Matsumura; Toshihiro Shimizu; Atsuo Shioda; Miki Kaneko; Kouji Miyazawa; Hajime Miyata; Naohide Tanaka; Toshikazu Uchida; Yasuyuki Arakawa

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 339 KB
• Volume: 64
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.1020

✦ Synopsis

Abstract

The present investigation compared the histological findings in the liver of chronic hepatitis C patients who were or were not co‐infected with TT virus (TTV) to determine the histological and clinical characteristics of TTV infection. One hundred eighty patients with chronic hepatitis or liver cirrhosis type C were included in this study. Serum samples were tested for the presence of TTV DNA by a nested polymerase chain reaction. The liver biopsy specimen of each patient was examined, and scores were assigned to indicate the severity of each of the following features: inflammatory cell infiltration in the periportal, parenchymal, and portal areas; fibrous stage; lymphoid reaction in the portal area; portal sclerotic change; perivenular fibrosis; pericellular fibrosis; damage of bile duct; and irregular regeneration of hepatocytes. Sixty‐four (34.4%) of the 180 patients were positive for TTV DNA. The histological features of the liver and the blood biochemical parameters of the TTV DNA‐positive and TTV DNA‐negative patients, did not differ significantly except for the score of irregular regeneration (IR) of hepatocytes. Among those in the F4 stage of fibrosis, the score of IR of the TTV DNA‐positive patients was significantly higher than that of the TTV DNA‐negative patients. In conclusion, chronic TTV infection does not modify the biochemical features of chronic hepatitis type C patients. TTV may be a risk factor, however, for the development of hepatocellular carcinoma in patients with type C liver disease in the F4 stage. J. Med. Virol. 64:74–81, 2001. © 2001 Wiley‐Liss, Inc.