Anonymous asked in 社會與文化語言 · 1 decade ago


主題Analysis of the Role of Autophagy in Replication of Herpes

Simplex Virus in Cell Culture

內容The herpes simplex virus type 1 (HSV-1) neurovirulence gene

encoding ICP34.5 controls the autophagy

pathway. HSV-1 strains lacking ICP34.5 are attenuated in growth

and pathogenesis in animal models and in

primary cultured cells. While this growth defect has been attributed

to the inability of an ICP34.5-null virus

to counteract the induction of translational arrest through the PKR

antiviral pathway, the role of autophagy

in the regulation of HSV-1 replication is unknown. Here we show

that HSV-1 infection induces autophagy in

primary murine embryonic fibroblasts and that autophagosome

formation is increased to a greater extent

following infection with an ICP34.5-deficient virus. Elimination of

the autophagic pathway did not significantly

alter the replication of wild-type HSV-1 or ICP34.5 mutants. The

phosphorylation state of eIF2 and viral

protein accumulation were unchanged in HSV-1-infected cells unable

to undergo autophagy. These data show

that while ICP34.5 regulates autophagy, it is the prevention of

translational arrest by ICP34.5 rather than its

control of autophagy that is the pivotal determinant of efficient HSV-1 replication in primary cell culture.



1 Answer

  • 1 decade ago
    Best Answer

    Autophagy 的角色的??Analysis 在Herpes 單工通信制病毒的複製在細胞培養

    ??The herpes 單工通信制病毒第一類型(HSV-1) neurovirulence 基因內碼ICP34.5 控制autophagy 路。HSV-1 張力缺乏ICP34.5 變稀在成長和發病原理在動物模型中和在主要被開化的細胞裡。當這個成長瑕疵歸因於ICP34.5 空病毒的無能抵制平移拘捕的歸納通過PKR 抗病毒路, 角色的autophagy 在HSV-1 複製的章程是未知的。這裡我們表示, HSV-1 傳染導致autophagy 在主要鼠科胚胎成纖維細胞並且, autophagosome 形成增加到一個更加了不起的程度跟隨傳染與ICP34.5 短少病毒。autophagic 路的排除極大沒有修改狂放類型HSV-1 或ICP34.5 突變體的複製。eIF2 phosphorylation 狀態和病毒蛋白質儲積是未改變的在HSV 1 被傳染的細胞裡無法接受autophagy 。這資料表示, 當ICP34.5 調控autophagy, 這是平移拘捕的預防由ICP34.5 而不是它的控制autophagy 是高效率的HSV-1 複製舉足輕重的定列式在原電池文化

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