The Role Of Stress Granules In The Process Of Newcastle Disease Virus Infection

In the course of virus infection, virus genome and protein produced by virus replication initiate innate immunity signaling pathway, leading to interferon secretion and interferon to stimulate gene expression and ultimately establish an antiviral state. Meanwhile, virus infection also induce stress granule(SG) containing ribonucleoprotein, RNA binding protein and eukaryotic initiated factors, etc. Innate immunity and SG are both cellular antiviral response. Correspondingly, virus promotes its own replication through inhibiting SG formation and innate immunity. SG contains RNA binding protein and a series of virus or host RNA, while the molecule associated to innate immunity such as pattern recognition receptor also specifically recognize virus RNA, indicating their close relationship. This paper will focus on the strategies to concernity how SG and innate immunity collaboratively exert antiviral function.Stimulation can induce the production of SG, which can be divided into two types: physical and chemical stimulation and virus infection. After a series of experiments, we conclusion that.Negative strand RNA virus NDV through the replication process generated double stranded RNA to active PKR/eIF2αpathway phosphorylation, resulting in SG. When a new synthesis of microtubules, will be more conducive to the activity of SG and increase the polymerization of SG, the morphology of SG becomes larger. That is to say, the microtubule has no effect on the formation of small SG stimulated by ARS, but for NDV inducing the formation of a relatively large form of SG plays a complementary role. Cycloheximide(CHX), drug of translation inhibition,intracellular protein can be used as identification of SG nature, through the identification, SG induced by NDV was classic, wrapped in a stagnation of the small ribosomal subunit and translation initiation factor. NDV induced the formation of SG.When TIA-1 and TIAR interferenced, the total protein synthesis increased translation; NP protein was reduced; the virus titer decreased, and the late changes in the infection was significant. SG induced by NDV was conducive to virus replication, including host mRNA,which possibly competes for translating virus proteins and host proteins.