Project/Area Number |
05454115
|
Research Category |
Grant-in-Aid for General Scientific Research (B)
|
Allocation Type | Single-year Grants |
Research Field |
Basic veterinary science/Basic zootechnical science
|
Research Institution | Hokkaido University |
Principal Investigator |
ONUMA Misao Hokkaido University, Faculty of Vet.Med., Professor, 獣医学部, 教授 (70109510)
|
Co-Investigator(Kenkyū-buntansha) |
SUGIMOTO Chihiro Hokkaido University, Faculty of Vet.Med., Assoc. Professor, 獣医学部, 助教授 (90231373)
|
Project Period (FY) |
1993 – 1994
|
Project Status |
Completed (Fiscal Year 1994)
|
Budget Amount *help |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 1994: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥4,600,000 (Direct Cost: ¥4,600,000)
|
Keywords | Theileria parasite / Piroplasm / Evasion mechanism / PCR / Parasite genotype / バキュロウイルス発現率 / アミノ酸置換 |
Research Abstract |
Cattle in Japan have been found to be infected with Theileria sergenti. Antigenic polymorphism has been demonstrated among stocks or field isolates of T.sergenti by using monoclonal antibodies. The results of Southern blot hybridization have also shown the genomic diversity of T.sergenti isolates. As one of the mechanisms that the parasitic protozoa evade host immune responses, they are known to express surface molecules with variant antigenic forms. This antigenic variation is related to change at genomic level, point mutatation, deletion or gene rearrangement in malaria and trypanosomes. To understand the evasion mechanism of T.sergenti, we analyzed one of the major surface proteins of merozoites (p32). We isolated 3 clones from cDNA library and nucleotide sequences were determined. Comparison of nucleotide sequences reveals at least 3 genetically different parasite population may coexist, and that transition of predominant parasite populations might occur during persistent infection. We further analyzed p32 antigenic difference of parasites obtained from different parasitemia peaks. Antigenic differences were observed among parasites from different peaks during persistent infection. There is a good correlation between the genotype changes and antibody responses. Population change in vivo indicates one of the parasite evasion mechanisms from host immune responses, because genetically different population may express antigenically different surface molecules.
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