Apoptotic events induced by human rhinovirus infection
Apoptotic events induced by human rhinovirus infection
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DOI：
10.1099/vir.0.80754-0
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发表时间：
2005-05-01
影响因子：
3.8
通讯作者：
Seipelt, J
中科院分区：
文献类型：
--
作者：
Deszcz, L;Gaudernak, E;Seipelt, J
感染人鼻病毒血清型14（HRV14）的HeLa和16HBE1 4o(-)支气管上皮细胞表现出典型的凋亡形态学改变，如细胞收缩和核固缩。这些事件与高分子量 DNA 断裂、caspase-9 和 caspase-3 的激活以及聚 (ADP-核糖) 聚合酶裂解同时发生。 Caspase 激活之前，细胞色素 c 从线粒体易位到细胞质，表明 HRV14 感染引起的细胞凋亡主要通过线粒体途径触发。细胞凋亡本身并不影响 HRV14 复制，但它促进了新形成的病毒从细胞中的释放。由于细胞凋亡在子代 HRV14 最大积累时被完全诱导，因此推测细胞凋亡导致细胞不稳定并促进病毒子代释放。
HeLa and 16HBE1 4o(-) bronchial epithelium cells infected with human rhinovirus serotype 14 (HRV14) were found to exhibit typical apoptotic morphological alterations, such as cell contraction and nuclear condensation. These events coincided with high-molecular-weight DNA fragmentation, activation of caspase-9 and caspase-3 and poly(ADP-ribose) polymerase cleavage. Caspase activation was preceded by cytochrome c translocation from the mitochondria to the cytoplasm, indicating that apoptosis caused by HRV14 infection was triggered predominantly via the mitochondrial pathway. Apoptosis did not affect HRV14 replication per se, but it facilitated the release of newly formed virus from cells. As apoptosis was fully induced at the time of maximal accumulation of progeny HRV14, it is postulated that apoptosis contributed to the destabilization of the cell and facilitated viral progeny release.