Host and vector manipulation following multi-infection of aphid transmitted viruses in sugar beet (Beta vulgaris)

在甜菜（Beta vulgaris subsp. vulgaris），病毒性黄化（VY）病是由不同蚜虫传播的病毒物种的复合体引起的，其中桃蚜是最重要的媒介。在欧洲，甜菜黄化病毒（BYV）、甜菜轻度黄化病毒（BMYV）、甜菜退绿病毒（BChV）和甜菜花叶病毒（BtMV）是甜菜病害的主要病原体，它们不仅以单一感染，而且以共感染和多重感染的方式阻碍甜菜的种植。已知共感染病毒在许多植物物种中增强至少一种所涉及的病毒的复制、组织传播、载体传播速率和其他适合度组分，并影响病毒性质，如宿主范围、细胞向性和载体偏好。此外，密切相关的病毒的多重感染是RNA重组的起点，启动新的、通常更具毒性的毒株或病毒种的形成。由于不能指望在Beta基因库中获得天然的多病毒抗性，并且通过杀虫剂处理减少病媒种群的常规病毒控制被禁止，因此迫切需要控制该疾病的替代解决方案。考虑到这一点，我们的项目旨在了解宿主共定殖过程中的病毒相互作用以及通过多重感染改变的载体相互作用，并可能分别对植物产生影响和增加传播。在病毒-植物水平上，我们的目标是破译推定的协同相互作用，通过转录组学鉴定所涉及的植物蛋白，并表征由黄化病毒在单一感染中操纵的代谢途径-与选定的共同/多重感染相比。在病毒感染对病媒操纵的水平上，应确定和量化对蚜虫行为的影响以及混合感染中病毒传播的偏好。该项目的主要成果是更好地了解在多重感染情况下病理系统（植物-病毒-载体）三个组成部分之间的紧密相互作用，这是一个生物现实。最终，该项目有可能确定未来控制措施的目标，这些措施将是安全和环保的。

In sugar beet (Beta vulgaris subsp. vulgaris), virus yellows (VY) disease is caused by a complex of different aphid-transmitted virus species, with Myzus persicae being the most important vector. In Europe, beet yellows virus (BYV), beet mild yellowing virus (BMYV), beet chlorosis virus (BChV) and beet mosaic virus (BtMV) are the main causatives and were shown to hamper sugar beet cultivation not only in single but also in co- and multi-infection. Co-infecting viruses are known in many plant species to enhance replication, tissue spread, vector transmission rate and other fitness components of at least one of the viruses involved and influence viral properties such as host range, cellular tropism and vector preference. Furthermore, multi-infection of closely related viruses is the starting point for RNA recombination initiating the formation of new, often more virulent strains or virus species. As natural multi-virus resistance cannot be expected to be available in the Beta genepool and conventional virus control by reducing vector populations through insecticide treatment was banned, alternative solutions controlling the disease are urgently required. Having this in mind, our project aims to understand viral interactions during host co-colonization as well as vector interactions that are altered by multi-infections and might acerbate impact on plants and increase transmission, respectively. On the virus-plant level, we aim to decipher putative synergistic interactions, identify by transcriptomics plant proteins involved and characterize metabolic pathways that are manipulated by the yellowing viruses in single- compared to selected co-/multi-infections. On the level of vector manipulation by the virus infection, effects on aphid behaviour as well as virus transmission preferences in co-infections shall be identified and quantified. The major outcome of this project is a better understanding of the tight interactions between the three components of the pathosystem (plant-virus-vector) in a multi-infection context, which is a biological reality. Ultimately, this project could potentially identify targets for future control measures that will be safe and environmentally friendly.