1988 Fiscal Year Final Research Report Summary
Studies on the major histocompatibility antigens as a factor determining the susceptibility to virus infection
| Project/Area Number |
62480159
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Virology
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| Research Institution | Shiga University of Medical Sciensce (1988)
Kyoto University (1987) |
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Principal Investigator |
SETO Akira Department of Microbiology, Shiga University of Medical Science, 医学部, 教授 (00025636)
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| Co-Investigator(Kenkyū-buntansha) |
熊谷 啓子 京都大学, 医学部, 教務職員
KAWANISHI Michiko Department of Microbiology, Kyoto University School of Medicine, 医学部, 助手 (60025616)
KUMAGAI Keiko Department of Microbiology, Kyoto University School of Medicine
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| Project Period (FY) |
1987 – 1988
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| Keywords | ATL / Histocompatibility antigen / HTLV-1 / 家兎 |
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| Research Abstract |
We succeeded in inducing fulminant ATL-like disease as well as a preleukemic stage of this disease in inbred rabbits. This animal model closely resembled human ATL and seemed to facilitate studies on immunological aspects of the disease. In the course of establishing this animal model, we made an observation that some offspring from an HTLV-l carrier doe were seroconverted, while other littermates from the same doe were not. We examined the correlation between the seroconversionand the haplotype of the major histocompatibility complex (MHC), hypothesizing that the MHC plays a major role in the HTLV-l infection and anti-virus antibody response. No close linkage was observed between the MHC haplotype and the seroconversion, but an apparent correlation was observed between the seroconversion and the genetic traits of B/J strain. The neonatal inoculation of HTLV-l producing cells from B/J strain induced no antibody response in the same strain, but induced a response in Chbb:HM strain. A similar inoculation of HTLV-l producing cells from Chbb:HM strain induced an antibody response in both of the strains. lnvestigation of such an unresponsiveness revealed that neonatal infection of HTLV-l could result in immunological tolerance to the virus antigens, thereby leading to a persistent infection without antibody formation.
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