Molecular biological analysis of the pathogenesis of human herpesviruses

分析了单纯疱疹病毒(HSV)、EB病毒(EBV)、巨细胞病毒(CMV)和人类疱疹病毒6型(HHV-6)致病的分子基础。阐述了CPE体外变异株(NiI)的选择能力、GC阴性突变体的分子基础(Mori)、US3蛋白激酶突变体(Nishiyama)的致病机制、氧化电位水(Shimizu)的抗疱疹作用、常见病例的分子流行病学(Sakaoka)以及各血清型的特异性核苷酸序列(Kurimura)。对于EBV，分析了与原发性胃癌(Osata)的病因学关系，分子再激活的分子开关机制(Takata)，以及DNA复制和基因表达(Hirai)。对CMV在免疫受损宿主(Minamishima)中的致病机制、在人体组织中的持续/潜伏感染模式(Furukawa)、视网膜色素上皮细胞(Kurata)的体外潜伏模型进行了研究。对于HHV-6和HHV-7，A型和B型HHV-6(Yamanishi)之间存在基因组变异，从唾液样本中频繁分离HHV-7(Mori)，以及HHV-7感染细胞(Nii)的超微结构特征。

Molecular basis of the pathogenesis of herpes simplex virus(HSV), Epstein-Barr virus(EBV), cytomegalovirus(CMV), and human herpesvirus 6(HHV-6) was analyzed in this project. For HSV, selective powers of CPE variants in vitro(Nii), molecular basis of gC negative mutants (Mori), pathogenesis of US3 protein kinase mutants (Nishiyama), antiherpetic effects of electrolyzed oxidizing water(Shimizu), molecular epidemiology of familiar cases (Sakaoka), and nucleotide sequences specific for each serotype (Kurimura) were clarified. For EBV, etiological relationship to primary gastric carcinomas (Osata), molecular switching mechanism for reactivation (Takata), and DNA replication and gene expression (Hirai) were analyzed. For CMV, pathogenesis in immuno-compromised hosts (Minamishima), mode of persistent/latent infections in human tissue (Furukawa), in vitro latency model in retinal pigment epitherial cells (Kurata) were studied. For HHV-6 and -7, genomic variation between types A and B of HHV-6 (Yamanishi), frequent isolation of HHV-7 from saliva samples (Mori), and ultrastructural vcharacteristics of HHV-7 infected cells (Nii) were demonstrated.