Development of influenza live vaccine by reverse genetics
Project/Area Number |
13557023
|
Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 展開研究 |
Research Field |
Virology
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Research Institution | The University of Tokyo |
Principal Investigator |
KAWAOKA Yoshihiro University of Tokyo, IMS, Professor, 医科学研究所, 教授 (70135838)
|
Co-Investigator(Kenkyū-buntansha) |
HORIMOTO Taisuke University of Tokyo, IMS, Associate Professor, 医科学研究所, 助教授 (00222282)
GOTO Hideo University of Tokyo, IMS, Assistant Professor, 医科学研究所, 助手 (50323639)
TAKADA Ayato University of Tokyo, IMS, Assistant Professor, 医科学研究所, 助手 (10292062)
OSUMI Kunio The Chemo-Sero Therapeutic Research Institute, The director, 第一製剤部長
|
Project Period (FY) |
2001 – 2002
|
Project Status |
Completed (Fiscal Year 2002)
|
Budget Amount *help |
¥14,100,000 (Direct Cost: ¥14,100,000)
Fiscal Year 2002: ¥6,100,000 (Direct Cost: ¥6,100,000)
Fiscal Year 2001: ¥8,000,000 (Direct Cost: ¥8,000,000)
|
Keywords | influenza virus / reverse genetics / live vaccine / A型インフルエンザウイルス / M2膜蛋白質 / M2蛋白質 / 膜貫通領域 |
Research Abstract |
Influenza virus is a highly infectious respiratory pathogen of birds and mammals, including human. It often produces significant mobidity and mortality in humans. Current methods of immunization against influenza virus include parental administration of inactivated influenza virus vaccines, which reduces the incidence of clinical illness in healthy subjects. But in some cases, immunization with inactivated vaccines is associated with very low protection rates or short protection periods. Another promising approach to vaccination is the use of live-attenuated influenza viruses. Theses vaccines have shown considerable promise in ongoing clinical trials. However, it has been concerned that the pathogenesis happened to recovered during their replication. We propose an alternative approach to the design of live virus vaccines, one that relies on alteration of the influenza A virus M2 protein which is responsible for ion channel activity. It did not show appreciable growth defect in cell culture, although its growth was attenuated in mice. It has shown that this M2 ion channel defective mutant virus protected mice against challenge with lethal doses of influenza virus, indicating the potential or incorporating this M2 alteration in a live influenza vaccine as one of the attenuating mutations.
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Report
(3 results)
Research Products
(15 results)