Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/66265
標題: 假性狂犬病毒感染細胞後蛋白質合成之研究
Protein synthesis in pseudorabies virus-infected cells
作者: 顏永仁
Yen, Yong-Ren
關鍵字: pseudorabies virus;假性狂犬病毒;protein synthesis;蛋白質合成
出版社: 獸醫微生物學研究所
摘要: 
假性狂犬病毒(pseudorabies vurus,PRV)是屬於阿爾法泡疹病毒(α-
herpesvirus),主要引起豬假性狂犬病(Aujeszky's disease),造成幼豬
中樞神經系統高頻率地致死性感染。跟單純泡疹病毒(herpes simplex
viruses)一樣,假性狂犬病毒亦能抑制宿主細胞的 DNA、RNA、與蛋白質
等大分子之合成作用,而本論文主要是著重在蛋白質合成之抑制作用。
MDBK或 LM細胞受到 PRV感染,雖然感染早期仍以細胞的蛋白質為主,但
是隨著感染時間的加長,細胞的蛋白質合成逐漸受到抑制,而以病毒特有
的蛋白質取而代之;而此種抑制作用可被2-aminopurine(2-AP)或
adenine部分回復,但無法被 poly(I)poly(C)或 interferon所影響;實
驗結果顯示了,2-AP與 adenine具有部分逆轉 PRV抑制作用之功能,而
poly(I)poly(C)與 interferon則不具抗 PRV病毒感染之作用。PKR(RNA-
dependent protein kinase)是一與細胞抗病毒作用有關之 protein
kinase;根據前人研究,病毒常會降低 PKR的表現量。而我們的結果顯示
,PRV亦能降低此 kinase的表現量及其磷酸化狀態。另外,在感染晚期,
PRV會降低間接參與轉譯作用之蛋白質 ERK-2(extracellular signal-
regulated kinase 2)的表現量。然而,也有某些蛋白質在受到病毒感染
下,仍會繼續表達,heat shock proteins(HSPs)即是其中最常被研究之
一;而我們的實驗結果亦顯示,不管是在感染早期或晚期,HSP70的表現
均不受 PRV影響,且進一步實驗結果顯示,此現象應是 PRV感染後,
HSP70的基因表現仍持續進行所致。

Pseudorabies virus(PRV),a member of alphaherpesviruses,is
the causing agent of Aujeszky's disease of pigs. Like herpes
simplex viruses,PRV can inhibit the synthesis of cellular
macromolecules,including DNA, RNA and protein,in lytic
infection. The impact of virus on host protein synthesis is the
theme of this study. In PRV-infected cells,the cellular protein
synthesis is shut-off gradually and virus-specific proteins ars
produced. The inhibition of host protein synthesis in PRV-
infected cells can be partially reversed by 2-aminopurine(2-AP)
or adenine. Although interferons have been well known for their
antiviral effects,the anti-PRV effect of interferon is not
observed in our study. The expression of RNA-dependent protein
kinase(PKR),a key player in the control of translational
initiation,is downregulated in late time of infection;and it is
found to be less phosphorylated. In addition,the western
blotting results show that the total amount of extracellular-
regulated kinase(ERK-2),which may participate translation
indirectly,is also decreased in late time of infection. Lastly,
our results reveal that heat shock protein 70(HSP 70) are
prevented from virus-induced shut-off by unknown mechanisms,and
the implications are discussed.
URI: http://hdl.handle.net/11455/66265
Appears in Collections:微生物暨公共衛生學研究所

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