Animal model of chronic hepatitis using duck hapatitis B virus precore mutant infection.
Project/Area Number |
09670511
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | Chiba University |
Principal Investigator |
TAGAWA Masami Chiba University, School of Medicine, Hospital, First Department of Medicine, Assistant, 医学部附属病院, 助手 (90261916)
|
Co-Investigator(Kenkyū-buntansha) |
YOKOSUKA Osamu Chiba University, School of Medicine, First Department of Medicine, Lecturer, 医学部, 講師 (90182691)
|
Project Period (FY) |
1997 – 1998
|
Project Status |
Completed (Fiscal Year 1998)
|
Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
|
Keywords | duck hepatitis B virus / precore mutant / animal model |
Research Abstract |
To analyze the function of precore protein and e antigen of hepatitis B virus, experimental infection of duck hepatitis B virus (DHBV) was performed and replicability and pathogenesis of precore mutant was investigated. Cloned DHBV DNA of 2 strains of wild type and 6 strains of precore defective mutant were transfected into the duck liver, and infectivity of virus and quantity of viral nucleic acids in the serum and the liver were compared. At 14 days of inoculation, infectivity of wild and precore mutant was 100% and 55%, respectively, and the amount of DHBV DNA in the serum was less in the carriers of precore mutant than wild type. Co-infection of wild and precore mutant DHBV resulted wild type viremia indicating that precore protein might facilitate the viral replication. Chronic infection of wild type showed high titer of viremia and minimal change of liver histology, whereas the replication of precore mutant was suppressed with the histological change of hepatocytes necrosis and intralobular lymphocytes infiltration. DHBc antigen expression was detected in all hepatocytes of wild and precore mutant carriers at 6 weeks of inoculation, and less amount of DHBc antigen in less number of hepatocytes was detected of precore mutant carriers at 20 weeks of inoculation. Chronic DHBV precore mutant infection accompanied with the immunological reaction and the suppression of virus replication. Precise investigation of virus related proteins has to be done to clarify the pathogenesis of precore mutant.
|
Report
(3 results)
Research Products
(2 results)