title: Serologically silent hepatitis B virus coinfection in patients with hepatitis C virus-associated chronic liver disease: clinical and virological significance.
abstract: Frequent coinfection of surface antigen-negative hepatitis B virus (silent HBV) in hepatitis C virus (HCV)-associated chronic liver disease (CLD) has been reported. The clinical and virological significance of silent HBV infection was investigated in 65 patients with HCV-associated CLD who subsequently received interferon (IFN) therapy. HBV DNA was detected in 34 (52.3%) patients by a nested polymerase chain reaction (PCR). Virologically, all of the 34 patients were found to have HBV with an eight-nucleotide deletion in the core promoter. Coinfection of silent HBV was more frequent with HCV genotype 1b than in 2a (64.3% vs. 28.6%, P<.01). With HCV genotype 1b, the serum RNA level was significantly higher (> or =10(6) copies per milliliter vs. < or =10(5) copies per milliliter) in patients with silent HBV than those without coinfection (P<.01). Clinically, silent HBV was associated with a higher level of serum alanine aminotransferase (158.5+/-104.8 vs. 121.8+/-78.6 IU/I; mean +/- SD) and a greater histological activity of hepatitis as evaluated by histological activity index score (9.4+/-3.8 vs. 8.6+/-4.5; mean +/- SD), although it was not statistically significant. Silent HBV was also associated with poor efficacy of IFN therapy (P<.01). The results suggest that silent HBV has some promoting effect for HCV replication, at least for HCV genotype 1b, and may affect the histological activity of hepatitis and IFN response in HCV-associated CLD.
authors.affiliation: 2nd Department of Internal Medicine, Shimane Medical University, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Fukuda
authors.forename: N
authors.initials: N
authors.lastname: Ishimura
authors.forename: M
authors.initials: M
authors.lastname: Niigaki
authors.forename: S
authors.initials: S
authors.lastname: Hamamoto
authors.forename: S
authors.initials: S
authors.lastname: Satoh
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: Y
authors.initials: Y
authors.lastname: Kushiyama
authors.forename: Y
authors.initials: Y
authors.lastname: Uchida
authors.forename: S
authors.initials: S
authors.lastname: Ihihara
authors.forename: S
authors.initials: S
authors.lastname: Akagi
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: Y
authors.initials: Y
authors.lastname: Kinoshita
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood / Q000187:drug effects; D000998:Antiviral Agents / Q000627:therapeutic use; D004279:DNA, Viral / Q000097:blood; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000187:drug effects / Q000235:genetics*; D006512:Hepatitis B Core Antigens / Q000097:blood; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000145:classification / Q000187:drug effects / Q000235:genetics*; D019694:Hepatitis B, Chronic / Q000097:blood* / Q000150:complications; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000821:virology; D006801:Humans; D007372:Interferons / Q000627:therapeutic use; D008099:Liver / Q000187:drug effects / Q000473:pathology / Q000821:virology; D008297:Male; D008875:Middle Aged; D011401:Promoter Regions, Genetic / Q000235:genetics; D012367:RNA, Viral / Q000097:blood
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D006512:Hepatitis B Core Antigens; D006514:Hepatitis B Surface Antigens; D012367:RNA, Viral; D007372:Interferons; D000410:Alanine Transaminase