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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Induction of apoptosis accelerates reactivation of latent HSV-1 in ganglionic organ cultures and replication in cell cultures
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Induction of apoptosis accelerates reactivation of latent HSV-1 in ganglionic organ cultures and replication in cell cultures

机译：诱导细胞凋亡可加快神经节器官培养物中潜在HSV-1的再激活和细胞培养物中的复制

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摘要

Herpes simplex viruses replicate at the portal of entry into the body and are transported retrograde to sensory neurons in which they can establish a silent, latent infection characterized by the expression of a noncoding latency-associated transcript and a set of microRNAs. At the portal of entry into the body and in cell culture a viral protein, VP16, recruits cellular proteins that initiate a sequential derepression of several kinetic classes of viral genes. Earlier studies have shown that upon reactivation of latent virus in ganglionic organ cultures all genes are derepressed at once, thus obviating the need for VP16 to initiate sequential derepression of viral genes. One hypothesis that could explain the data is that the massive reactivation of all classes of viral genes is the consequence of activation of an apoptotic pathway. Here we show that two proapoptotic drugs, dexamethasone and 2[[3-(2,3-dichloro-phenoxy)propyl]amino]-ethanol, each accelerates viral gene expression in ganglionic organ cultures. We also show that in cultured cells apoptosis induced by dexamethasone accelerates viral gene expression and accumulation of infectious virus. The results are surprising in light of the relatively large number of viral proteins that independently block apoptosis induced by viral gene products or exogenous agents. The results suggest that the virus may rely on apoptosis to exit from latency but that apoptosis may be detrimental for virus replication or spread at the portal of entry into the body.
机译：单纯疱疹病毒在进入人体的门户处复制并逆行转运至感觉神经元，在其中它们可以建立沉默，潜伏的感染，其特征是与非编码潜伏期相关的转录本和一组微RNA的表达有关。在进入人体和细胞培养的门户中，病毒蛋白VP16募集了细胞蛋白，这些蛋白启动了病毒基因几个动力学类别的顺序去阻遏作用。早期的研究表明，在神经节器官培养物中重新激活潜伏病毒后，所有基因都会立即被抑制，从而消除了对VP16启动病毒基因顺序抑制的需求。可以解释该数据的一种假设是，所有类别的病毒基因的大量重新激活是凋亡途径激活的结果。在这里，我们显示了两种促凋亡药物，地塞米松和2 [[[3-（2,3-二氯-苯氧基）丙基]氨基]-乙醇，每个都在神经节器官培养物中加速病毒基因的表达。我们还表明，在培养的细胞中，地塞米松诱导的细胞凋亡会加速病毒基因的表达和感染性病毒的积累。鉴于相对大量的病毒蛋白可独立阻断由病毒基因产物或外源性试剂诱导的凋亡，因此结果令人惊讶。结果表明，病毒可能依赖于凋亡来避免潜伏期，但是凋亡可能对病毒复制或在进入人体的门户处扩散有害。

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