Hantaviruses are maintained by persistently infected rodents,with incidental infection of humans.Previous work about the long-term infected Vero-E6 cell cultures by Seoul virus (SEOV) showed that deletions at the 3' termini of virus RNAs accumulated during the infection,which may play an important role for virus persistence infection.However,changes of SEOV RNA rodent hosts and patients naturally infected were not clear.In this study,total RNA was extracted from blood clot of SEOV positive patients and lung tissues of SEOV positive Rattus norvegicus captured in field respectively.Variability of the termini of SEOV S segment was determined by RNA sequences from different clones,and modeled for secondary RNA structures.Termini diversity could be detected for SEOV S sequence from natural infected rodent hosts and patients.There were 5' end,3'end and both ends nucleotide sequence deletions observed,especially the typical types of DI RNAs (RNAs with large genome deletions) at both ends could be detected in rodent hosts,which was distinct from what was observed in long-term Vero-E6 cell cultures,in which only short 3' terminal sequence missing could be detected.While,diversities for clones from patients was lower than that from rodent hosts,except for one clone from a patient had 3' end nucleotide missing.Secondary RNA structures deduced from clones with different termini sequence missing changed significantly,Variations of terminal sequences from rodent hosts appeared to be distinctive with those from patients,which might attribute to the influences by host factors and it might be important to viral persistence in rodent hosts.%在汉城型汉坦病毒(Seoul virus,SEOV)长期感染的Vero-E6细胞过程中发现,病毒在持续感染过程中存在RNA3’末端序列缺失现象,可能对病毒的持续感染有重要作用.而自然感染的宿主动物或病人体内病毒RNA末端序列的变异情况并不清楚.本文从SEOV感染的病例血块以及SEOV检测阳性的褐家鼠肺组织中提取RNA,测定病毒S片段末端序列,并进行RNA二级结构模拟.结果发现,自然感染的宿主动物褐家鼠体内的SEOV S片段5’末端、3’末端及双末端均可出现序列缺失,而感染病例体内的病毒仅在一个克隆检测到3’末端序列缺失.与长期感染的Vero-E6细胞感染模型中仅存在较短的3’末端序列缺失现象不同,宿主动物的克隆既有较短的3’末端序列缺失,也有5’末端和双末端序列缺失,另外还有典型的大片段序列缺失.不同序列缺失类型的RNA序列二级结构模型存在显著差异.自然感染的宿主动物和病人体内的SEOV S片段序列末端存在序列缺失多样性,但前者的多样化程度更高.因此我们认为这些序列缺失可能受宿主因素影响,并与病毒对宿主的持续感染相关.
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