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Virus-mediated suppression of host non-self recognition facilitates horizontal transmission of heterologous viruses

机译:病毒介导的对宿主非自我识别的抑制促进了异源病毒的水平传播

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Non-self recognition is a common phenomenon among organisms; it often leads to innate immunity to prevent the invasion of parasites and maintain the genetic polymorphism of organisms. Fungal vegetative incompatibility is a type of non-self recognition which often induces programmed cell death (PCD) and restricts the spread of molecular parasites. It is not clearly known whether virus infection could attenuate non-self recognition among host individuals to facilitate its spread. Here, we report that a hypovirulence-associated mycoreovirus, named Sclerotinia sclerotiorum mycoreovirus 4 (SsMYRV4), could suppress host non-self recognition and facilitate horizontal transmission of heterologous viruses. We found that cell death in intermingled colony regions between SsMYRV4-infected Sclerotinia sclerotiorum strain and other tested vegetatively incompatible strains was markedly reduced and inhibition barrage lines were not clearly observed. Vegetative incompatibility, which involves Heterotrimeric guanine nucleotide-binding proteins (G proteins) signaling pathway, is controlled by specific loci termed het (heterokaryon incompatibility) loci. Reactive oxygen species (ROS) plays a key role in vegetative incompatibility-mediated PCD. The expression of G protein subunit genes, het genes, and ROS-related genes were significantly down-regulated, and cellular production of ROS was suppressed in the presence of SsMYRV4. Furthermore, SsMYRV4-infected strain could easily accept other viruses through hyphal contact and these viruses could be efficiently transmitted from SsMYRV4-infected strain to other vegetatively incompatible individuals. Thus, we concluded that SsMYRV4 is capable of suppressing host non-self recognition and facilitating heterologous viruses transmission among host individuals. These findings may enhance our understanding of virus ecology, and provide a potential strategy to utilize hypovirulence-associated mycoviruses to control fungal diseases.
机译:非自我识别是有机体中的普遍现象。它通常会导致先天免疫,从而防止寄生虫入侵并维持生物的遗传多态性。真菌的营养不相容性是一种非自我识别的类型,通常会诱发程序性细胞死亡(PCD),并限制分子寄生虫的扩散。尚不清楚病毒感染是否会减弱宿主个体之间的非自我识别以促进其传播。在这里,我们报告说,一种与低毒力相关的mycoreovirus,名为核盘菌核盘菌mycoreovirus 4(SsMYRV4),可以抑制宿主非自我识别并促进异源病毒的水平传播。我们发现,SsMYRV4感染的核盘菌菌核菌菌株和其他测试的营养不相容菌株之间的混合菌落区域中的细胞死亡明显减少,并且未清楚观察到抑制弹幕。营养不相容性涉及异三聚体鸟嘌呤核苷酸结合蛋白(G蛋白)信号传导途径,受称为het(杂核不相容性)基因座的特定基因座控制。活性氧(ROS)在植物不相容性介导的PCD中起关键作用。在SsMYRV4的存在下,G蛋白亚基基因,het基因和ROS相关基因的表达显着下调,并且ROS的细胞产生受到抑制。此外,感染SsMYRV4的菌株可以通过菌丝接触轻松接受其他病毒,并且这些病毒可以有效地从感染SsMYRV4的菌株传播到其他营养不相容的个体。因此,我们得出结论,SsMYRV4能够抑制宿主非自我识别并促进异源病毒在宿主个体之间传播。这些发现可能会增强我们对病毒生态学的理解,并提供利用低毒力相关性分枝杆菌病毒控制真菌疾病的潜在策略。

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