Activation of heat-shock response by an adenovirus is essential for virus replication
Activation of heat-shock response by an adenovirus is essential for virus replication
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DOI：
10.1038/35025102
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发表时间：
2000-09-14
期刊：
影响因子：
64.8
通讯作者：
Cotten, M
中科院分区：
文献类型：
--
作者：
Glotzer, JB;Saltik, M;Cotten, M
成功的病毒感染需要病毒重定向宿主生物化学以复制病毒基因组，并产生和组装子代病毒粒子。细胞热休克反应，其特征是热休克蛋白的升高和重新定位，发生在许多病毒的复制过程中（1-7）。这种反应可能是宿主对外来蛋白合成的反应，也可能是病毒需要激活转录的无关后果。或者，由于热休克蛋白可以促进蛋白质折叠（8,9），激活热休克反应可能是确保病毒蛋白和病毒粒子适当合成的特定病毒功能。由于涉及的病毒基因（如Ad5 E1A，参考文献10）也控制着其他必要的复制步骤，因此不可能确定热休克反应是否是病毒复制所必需的。在这里，我们报道了由禽流感病毒CELO编码的蛋白Gam1的表达（参考文献11），可以升高hsp70和hsp40并使其重新定位。gam1阴性CELO是复制缺陷；然而，Gam1功能可以被热休克或强迫hsp40表达部分取代。因此，Gam1在病毒复制过程中的一个基本功能是以hsp40为主要靶点激活宿主热休克反应。
Successful viral infection requires viruses to redirect host biochemistry to replicate the viral genome, and produce and assemble progeny virions. Cellular heat-shock responses, which are characterized as elevation and relocalization of heat-shock proteins, occur during replication of many viruses(1-7). Such responses might be host reactions to the synthesis of foreign protein, or might be irrelevant consequences of the viral need to activate transcription. Alternatively, as heat-shock proteins can facilitate protein folding(8,9), activating a heat-shock response might be a specific virus function ensuring proper synthesis of viral proteins and virions. It is not possible to determine whether heat-shock response is essential for virus replication, because the implicated viral genes (such as Ad5 E1A, ref. 10) also control other essential replication steps. Here we report that expression of Gam1, a protein encoded by the avian virus CELO (ref. 11), elevates and relocalizes hsp70 and hsp40. Gam1-negative CELO is replication-defective; however, Gam1 function can be partially replaced by either heat shock or forced hsp40 expression. Thus, an essential function of Gam1 during virus replication is to activate host heat-shock responses with hsp40 as a primary target.