title: Alteration of infection pattern of duck hepatitis B virus by immunomodulatory drugs.
abstract: The relationship between host immune state and hepatic inflammation and infection pattern of the Duck hepatitis B virus (DHBV) was investigated by experimental transmission of DHBV into 98 Japanese 7-day-old ducklings that had been pretreated with immunoregulatory drugs including cyclophosphamide, OK 432, and a steroid hormone. Immunosuppressive treatment with cyclophosphamide revealed an extension of the viremic period associated with an absence of inflammatory changes in the liver. Although immunostimulating treatment with OK 432 showed a remarkable accumulation of inflammatory cells in the liver, the viremic period was not shortened. Treatment with a steroid used as a immunosuppressant did not suppress the hepatitis; moreover, it increased viral DNA replication and extended the viremic period. This phenomenon of viral replication seemed to be caused by the direct effects of the steroid. Alteration of DHBV infection by modifying the host immune state is quite similar to that of hepatitis B virus (HBV) in humans. In DHBV infection, the host immune state seemed to have a considerable role in determining the infection pattern and degree of hepatitis activity. DHBV may be a helpful model of HBV for studying host-viral interaction and the immunological mechanism of viral hepatitis.
authors.affiliation: Second Department of Internal Medicine, Shimane Medical University, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Fukuda
authors.forename: S
authors.initials: S
authors.lastname: Okinaga
authors.forename: S
authors.initials: S
authors.lastname: Akagi
authors.forename: M
authors.initials: M
authors.lastname: Hidaka
authors.forename: N
authors.initials: N
authors.lastname: Ono
authors.forename: S
authors.initials: S
authors.lastname: Fukumoto
authors.forename: Y
authors.initials: Y
authors.lastname: Shimada
mesh_terms: D000276:Adjuvants, Immunologic / Q000494:pharmacology*; D000818:Animals; D002353:Carrier State / Q000276:immunology; D003520:Cyclophosphamide / Q000494:pharmacology; D004279:DNA, Viral / Q000096:biosynthesis; D004259:DNA-Directed DNA Polymerase / Q000378:metabolism; D004195:Disease Models, Animal; D004372:Ducks; D006509:Hepatitis B / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D006515:Hepatitis B virus / Q000187:drug effects / Q000502:physiology; D006524:Hepatitis, Viral, Animal / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D006854:Hydrocortisone / Q000031:analogs & derivatives / Q000494:pharmacology; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D010844:Picibanil / Q000494:pharmacology; D014766:Viremia / Q000276:immunology; D014779:Virus Replication / Q000187:drug effects
chemical_list: D000276:Adjuvants, Immunologic; D004279:DNA, Viral; D007166:Immunosuppressive Agents; D010844:Picibanil; D003520:Cyclophosphamide; D004259:DNA-Directed DNA Polymerase; C007133:hydrocortisone hemisuccinate; D006854:Hydrocortisone