Reassortment of Bunyavirus in ticks and animal models

项目总结/摘要 SFTSV被列为世界卫生组织最危险的九种病原体之一，其致死率为12-30%， 通过蜱对动物/人、人对人和动物对人传播， 一种具有血小板减少症特征免疫病原性疾病。病毒重组是一个过程 基因重组是分段RNA病毒所独有的， 天然宿主和载体与多种病毒的相互作用可能导致基因片段的改组， 产生具有新基因组组合的子代病毒。重组对病毒影响很大 适应性，并直接影响抗原变异，混淆了可用的病毒控制方法。在 在本申请中，我们将检验蜱介导的SFTSV感染的自然过程和 重配引起适应性、遗传性、抗原性或致病性的表型变化 转化为后代繁殖体。本研究的目的是展示SFTSV的自然过程 感染和重配，用于体外适应性、免疫原性、传播性和致病性 体内动物模型和H.长角蜱，最终将基础研究与临床 应用程序.

Project Summary/Abstract Listed in the WHO top nine most dangerous pathogens, SFTSV has 12-30% fatality rates, rapidly spreads through tick-to-animal/human, human-to-human and animal-to-human and induces immunopathogenic disease with a characteristic thrombocytopenia. Virus reassortment is a process of genetic recombination that is exclusive to segmented RNA viruses in which co-infection of a cell of natural host and vector with multiple viruses may result in the shuffling of gene segments to generate progeny viruses with novel genome combinations. Reassortment greatly affects virus fitness and directly influences antigenic variation, confounding available methods of virus control. In this application, we will test the hypothesis that tick-mediated natural course of SFTSV infection and reassortment introduces phenotypic changes of fitness, transmissibility, antigenicity, or pathogenicity into progeny reassortants. The goal of this study is to demonstrate the natural course of SFTSV infection and reassortment for fitness, immunogenicity, transmissibility, and pathogenesis in in vitro and in vivo animal models and H. longicornis ticks, ultimately bridging basic research to clinical application.