VARICELLA-ZOSTER VIRUS INDUCES APOPTOSIS IN CELL-CULTURE
VARICELLA-ZOSTER VIRUS INDUCES APOPTOSIS IN CELL-CULTURE
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DOI：
10.1099/0022-1317-76-11-2875
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发表时间：
1995-11-01
影响因子：
3.8
通讯作者：
REUTIER, B
中科院分区：
文献类型：
--
作者：
SADZOTDELVAUX, C;THONARD, P;REUTIER, B
细胞凋亡是一种活跃的细胞死亡机制，可在多种刺激（包括病毒感染）下启动。在这项工作中，我们证明了水痘-带状疱疹病毒（VZV），一种人类疱疹病毒的溶解性感染，其特征是DNA的核分裂成寡核体片段和染色质凝聚。在体外，vzv诱导的细胞死亡实际上是通过细胞凋亡介导的。细胞保护自身免受凋亡的机制可能是允许病毒潜伏期建立的参数之一。对于VZV，它可以潜伏在感觉神经节中，我们还没有发现一种细胞或病毒蛋白可以发挥这种保护作用，因为观察到的细胞凋亡机制似乎独立于Bcl-2，这是最常见的细胞凋亡抑制剂。
Apoptosis is an active mechanism of cell death which can be initiated in response to various stimuli including virus infections. In this work, we demonstrate that lytic infection by varicella-zoster virus (VZV), a human herpesvirus, is characterized by nuclear fragmentation of DNA into oligonucleosomal fragments and by chromatin condensation. In vitro, VZV-induced cell death is actually mediated by apoptosis. The mechanisms developed by cells to protect themselves against apoptosis could be one of the parameters allowing the establishment of virus latency. In the case of VZV, which can remain latent in sensory ganglia, we have not yet identified a cellular or viral protein which could play this protective role, since the observed apoptosis mechanism seems to be independent from Bcl-2, the most frequently described inhibitor of apoptosis.