先天免疫系统
转录组
生物
核糖核酸
微生物学
基因组
核糖体蛋白
病毒学
免疫系统
遗传学
基因
基因表达
核糖体
作者
Tao Li,Sheng Qin,Xia Sun,Kai-xiang Zhang,Xinyi Ding,Xueyang Wang,Muwang Li
标识
DOI:10.1016/j.aspen.2022.101938
摘要
We propose a schematic diagram for the early transcriptional responses between the susceptible and resistant silkworm strains after AcMNPV infection. In brief, when AcMNPV infect susceptible strains of silkworm, the inhibition of innate immunity and host translational machinery, as well as up-regulation of cytoskeleton, that these responses promote baculoviral BV transport and ingress into the nucleus, thus facilitating the replication of baculovirus. However, when AcMNPV infect resistant strains of silkworm, down-regulation of endocytosis and RNA transport weakened the ability of the baculoviral BV entry into the nucleus, while up-regulation of ribosomal proteins and energy metabolic to inhibit the replication of the virus. • Early transcriptional responses were analyzed in different resistant strains of silkworm to AcMNPV infection. • Distinct innate immunity and ribosomal response were found between the resistant and susceptible silkworm strains. • Provide basic data for the initial host transcriptional responses to viral infection in silkworm. Baculoviruses are enveloped rod-shaped viruses that with circular double-stranded and large DNA genome. Baculoviruses successfully invade by using the host factors, especially at the process of establishing early infection. In this study, we investigated the different resistant strains of silkworm in response to AcMNPV early infection by RNA-sequencing. Our data revealed that the genes involved in innate immunity and ribosomal proteins were suppressed and cytoskeleton were induced in susceptible strain p50, thus facilitating the viral replication. However, in resistant strain C108, the genes participated in endocytosis and RNA transport were down-regulated, while up-regulation of ribosomal proteins and energy metabolic to inhibit the infection of the virus. These data provide a new sight of the initial host transcriptional responses to viral infection in silkworm.
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