Host-parasite coevolutionary dynamics and the disease control

[1]分析了寄主植物和病原真菌在基因对基因互作下的协同进化动力学。从理论上评估了抗性小种的混合种植和对病原体的多重抗性的引入的效果（Sasaki A，Proc. R，Soc. Lond. B，2000年; Iwanaga A，Sasaki A，in review）.还研究了集合种群中基因对基因动态中出现的自发性突变（Sasaki A，汉密尔顿WD，Ubeda F，Proc. R. Soc. Lond. B，2002年）。[2]考虑到有限种群的随机漂移，研究了HIV和病原菌耐药性发展下的最佳药物治疗。还使用病毒表位的有限位点模型分析宿主中HIV的抗原漂移中随机漂移的影响（Haraguchi Y，Sasaki A，J. Mol. Biol. Evol.，2000年）。[3]本文根据脊髓灰质炎流行病学动力学、流行病学和流行病学资料，估计了口服脊髓灰质炎疫苗退出后，疫苗衍生强毒重新出现的可能性。 ...更多信息 从理论上讲，强毒病毒爆发的风险相当高（Haraguchi Y，Sasaki A，Yoshida H，Am. J. Epidem.审查中）。[4]提出了利用动物预防（将病媒蚊子吸引到疟疾的死宿主）的疟疾控制策略。在中间使用杀虫剂的情况下，可以根除疟疾而不允许在蚊子中产生杀虫剂抗性（川口I，Sasaki A，Mogi M，Proc. R. Soc. Lond. B，综述中）。[5]对登革病毒第二次感染时死亡率增加的特殊现象进行了建模，并从理论上分析了其对登革亚型稳定共循环的影响（川口I，Sasaki A，Boots M，Evolution，in review）。[6]分析了空间结构和接触网络结构（“小世界”效应）对毒力进化和流行病学动力学的影响（Haraguchi Y，Sasaki A，J. theor.生物学：2000; Boots M，Sasaki A，Ecology Letters，2000; Boots M，Sasaki A，Am.纳特，2002年）。[7]分析了具有季节性和交叉免疫的多菌株流行病学动态，以预测流行病爆发的模式（卡莫M，Sasaki A，Physica D，2002）。少

[1] Coevolutionary dynamics of host plant and fungus pathogen uder gene-for-gene interaction is analyzed. The effect of mixed planting of resistant races, and the introduction of multiple resistance against pathogens are theoretically evaluated (Sasaki A, Proc. R, Soc. Lond. B, 2000; Iwanaga A, Sasaki A, in review).Also investigated is the spontaneous asynchrony emerging in the gene-for-gene dynamics in metapopulation (Sasaki A, Hamilton WD, Ubeda F, Proc. R. Soc. Lond. B, 2002).[2] Optimal drug treatment under the development of drug resistance in HIV and pathogenic bacteria is studied taking into account the random drift due to a finite population. The effect of random drift in antigenic drift of HIV in a host is also analyzed using a finite site model for viral epitopes (Haraguchi Y, Sasaki A, J. Mol. Evol., 2000).[3] The probability of re-emergence of vaccine derived virulent virus after the secession of oral polio vaccination is estimated based on the epidemilological dynamics, wa … More ring theoretically that the risk of virulent virus outbreak is quite high (Haraguchi Y, Sasaki A, Yoshida H, Am. J. Epidem. in review).[4] Maralia control strategy is proposed which make use of the zooprolylaxis (the attraction of vector mosquitoes to an dead-end host of malaria). With an intermediate use of insecticide, the malaria can be eradicated without allowing the development of insecticide resistance in mosquitoes (Kawaguchi I, Sasaki A, Mogi M, Proc. R. Soc. Lond. B, in review).[5] A pecuriar phenomena of mortality enhancement at the second infection by dengue viruses is modeled, and its effect on the stable cocirculation of dengue subtypes is analyzed theoretically (Kawaguchi I, Sasaki A, Boots M, Evolution, in review).[6] The effect of spatial structure and the contact network structure ('small world' effect) on the evolution of virulence and the epidemiological dynamics is analyzed (Haraguchi Y, Sasaki A, J. theor. Biol., 2000; Boots M, Sasaki A, Ecology Letters, 2000; Boots M, Sasaki A, Am. Nat., 2002).[7] The multistrain epidemiological dynamics with seasonality and cross-immunity is analyzed to forecast the pattern of epidemic outbreaks (Kamo M, Sasaki A, Physica D, 2002). Less