Molecular analysis of parasitic adaptation in Malaria parasite

在疟疾疫苗的开发研究中，Horii博士分析了乌干达全流行区疟疾症状与抗重组SERA （SE47’蛋白）的血清IgG亚类之间的相关性。结果表明，抗se47 IgG3滴度高的人无疟疾热，外周血寄生虫率低。此外，纯化的抗se47’人IgG3在体外抑制了寄生虫的生长。这些结果有力地提示了基于重组SE47’蛋白（Horii）的疟疾疫苗的可行性。Matsuoka博士通过基因枪直接免疫小鼠杠杆的CSP基因，保护小鼠免受伯格黑氏杆菌的侵袭感染。Ohta博士确定了与人类HLA-DR结合的氨基酸寡核苷酸序列。Drs。Yamada和Kambara一直致力于在带有MSP1基因的小鼠模型上研究重组卡介苗疟疾疫苗。在对疟原虫寄生适应性的研究中，Tanabe博士证明了多态MSP1等位基因之间的连锁不平衡。他进一步提出，免疫选择是一种可能的机制，与疟疾爆发有关。Torii在小鼠模型中分离并分析了参与卵裂子侵入红细胞的Rhoptory蛋白基因。Urade博士对恶性疟原虫分泌前列腺素的机制进行了生化分析。

For the developmental study of malaria vaccine, Dr. Horii analyzed a correlation between malaria symptom and serum IgG subclass against the recombinant SERA (SE47' protein) in the holo-endemic area in Uganda. It was revealed that people with high anti-SE47' IgG3 titer showed no malaria fever and low parasitemia in the peripheral blood. In addition, the purified anti-SE47' human IgG3 inhibited the parasite growth in vitro. These results strongly suggest the feasibility of malaria vaccine based on the recombinant SE47' protein (Horii). Dr. Matsuoka protected mice against P. berghei challenge infection by a direct immunization of their lever with CSP gene by gene gun. Dr. Ohta identified oligo sequences of amino acids that bind to human HLA-DR. Drs. Yamada and Kambara has been working on the recombinant BCG malaria vaccine in mouse model with MSP1 gene.In the study of parasitic adaptation of malaria parasite, Dr. Tanabe demonstratd the linkage disequilibrium among polymorphic MSP1 alleles. He further suggeted the immune selection as a possible mechanism and the relation to malaria breakout.Dr. Torii has isolated and analyzed genes of Rhoptory proteins that function in merozoite invasion to erythrocyte in mouse model. Dr. Urade has conducted biochemical analysis of the mechanism for prostaglandin production in P. falciparum.