title: Relevance of inapparent coinfection by hepatitis B virus in alpha interferon-treated patients with hepatitis C virus chronic hepatitis.
abstract: The aim of the study was to investigate whether an "inapparent" coinfection by hepatitis B virus (HBV) in anti-HCV-positive chronic liver disease patients may influence interferon (IFN) response. Fourteen anti-HCV-positive, hepatitis B surface antigen (HBsAg)-negative but serum HBV-DNA-positive patients and 111 anti-HCV-positive, HBsAg-negative, and HBV-DNA-negative patients with chronic hepatitis were treated with 3 MU of recombinant alpha-2a IFN 3/week for 1.2 months. Serum HBV-DNA and HCV-RNA were determined before treatment, after 6-12 months, and at the time of alanine aminotransferase (ALT) flare-up by HBV polymerase chain reaction (PCR) and HCV PCR, respectively. IgM anti-HBc were tested using the IMx Core-M assay (Abbott Laboratories, North Chicago, IL). By the end of treatment, ALT values had become normal in 4/14 HBV-DNA-positive patients (28%), but all "responders" (4/4) relapsed. IgM anti-HBc was detected both before treatment and during ALT elevation in three patients and only during ALT relapse in another three. In the remaining 111 patients, a biochemical response to IFN treatment was observed in 54% and relapse of ALT values in 47%. "Inapparent" HBV/HCV coinfection may be implicated in cases of resistance to IFN. HBV replication and HBV-related liver damage may persist in patients in whom HCV replication was inhibited by current doses of IFN, as suggested also by the presence of IgM anti-HBc in some cases. Further studies will show the effect of different treatment schedules. HBV-DNA and/or IgM anti-HBc detection with very sensitive methods may be important both as a prognostic factor and as a tool for better understanding of intervirus relationships and mechanisms involved in multiple hepatitis virus infections.
authors.affiliation: Istituto Medicina Interna, University of Florence, Italy.
authors.forename: A L
authors.initials: AL
authors.lastname: Zignego
authors.forename: R
authors.initials: R
authors.lastname: Fontana
authors.forename: S
authors.initials: S
authors.lastname: Puliti
authors.forename: S
authors.initials: S
authors.lastname: Barbagli
authors.forename: M
authors.initials: M
authors.lastname: Monti
authors.forename: G
authors.initials: G
authors.lastname: Careccia
authors.forename: F
authors.initials: F
authors.lastname: Giannelli
authors.forename: C
authors.initials: C
authors.lastname: Giannini
authors.forename: G
authors.initials: G
authors.lastname: Buzzelli
authors.forename: M R
authors.initials: MR
authors.lastname: Brunetto
authors.forename: F
authors.initials: F
authors.lastname: Bonino
authors.forename: P
authors.initials: P
authors.lastname: Gentilini
mesh_terms: D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D000998:Antiviral Agents / Q000627:therapeutic use*; D002908:Chronic Disease; D004279:DNA, Viral / Q000097:blood; D005260:Female; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology; D006509:Hepatitis B / Q000150:complications / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D006515:Hepatitis B virus / Q000235:genetics / Q000276:immunology; D006526:Hepatitis C / Q000150:complications / Q000188:drug therapy* / Q000235:genetics; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D000410:Alanine Transaminase