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Characterization of hepatitis B virus mutant from patient with fulminant hepatitis.

Research Project

Project/Area Number 08670630
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Gastroenterology
Research InstitutionTokyo Women's Medical University

Principal Investigator

HASWGAWA Kiyoshi  Medical Department, Tokyo Women's Medical University, 医学部, 講師 (30172886)

Project Period (FY) 1996 – 1998
Project Status Completed (Fiscal Year 1998)
Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Keywordshepatitis B virus / fulminant hepatitis / mutant / animal model / 点突然変異 / 激症肝炎
Research Abstract

We established a mouse model of hepatitis B involving liposome-mediated gene transfer, aiming to compare the antibody response to viral DNA from a patient with fulminant hepatitis with the response to wild-type viral DNA. A mixture of liposomes and full-length viral DNA was injected intrahepatically. Three days after transfection, viral transcript and antigen were detected in the liver by reverse transcription-polymerase chain reaction and immunohistochemistry. Also on day 3, hepatitis B surface antigen became detectable in the circulation. At 7 days mice of an initially nonresponding strain were reinjected, and they developed demonstrable serum antibody against viral surface antigen 5 days later. The mice transfected with the fulminant hepatitis-associated DNA produced six times the amount of antibody produced by mice transfected wild-type viral DNA. No difference was observed in amount of viral transcript or antigen in the liver or amount of in circulating hepatitis B surface antigen, suggesting that the higher antibody production in mice transfected with fulminant hepatitis-associated viral DNA resulted from increased antigenicity rather than antigen quantity. Previous DNA sequence analysis has identified mutations producing four amino acid substitutions in the envelope region compared to the wild-type virus. One or more of these amino acid changes presumably incited the hyperimmune response in mice and possibly also the patient's fulminant clinical course.

Report

(4 results)
  • 1998 Annual Research Report   Final Research Report Summary
  • 1997 Annual Research Report
  • 1996 Annual Research Report
  • Research Products

    (2 results)

All Other

All Publications (2 results)

  • [Publications] Kato,J.,Hasegawa,K.et al.: "A molecular analysis of viral pensistence in surface antigen-negative chronic hepatitis B." Hepatology. 23. 389-395 (1996)

    • Related Report
      1996 Annual Research Report
  • [Publications] Baument,TF,Rogers,SA.,Hasegawa,K.,et al.: "Two core promotor mutations identified in a Hepatitis B virus strain associated with fulminant hepatitis result in enhanced viral replication" J.Clin.Invest.98. 2268-2276 (1996)

    • Related Report
      1996 Annual Research Report

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Published: 1996-04-01   Modified: 2016-04-21  

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