Enhanced in vitro reactivation of herpes simplex virus type 2 from latently infected guinea-pig neural tissues by 5-azacytidine.
Enhanced in vitro reactivation of herpes simplex virus type 2 from latently infected guinea-pig neural tissues by 5-azacytidine.
复制标题
5-氮杂胞苷增强潜伏感染豚鼠神经组织中 2 型单纯疱疹病毒的体外再激活。
DOI：
10.1099/0022-1317-69-5-1079
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Bernstein,DI
中科院分区：
文献类型：
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作者：
Stephanopoulos,DE;Kappes,JC;Bernstein,DI
5-氮杂胞苷 (5-AZC) 可减少 DNA 中的胞嘧啶甲基化，据报道可激活休眠病毒基因。用 5-AZC 体外处理潜伏单纯疱疹病毒 2 型 (HSV-2) 感染的豚鼠背根神经节和脊髓的外植体培养物，显着提高了 HSV 恢复率。在外植体培养物中添加 50 µM-5-AZC 后，神经节分离株数量 (P< 0.001) 和恢复率 (P< 0.001) 均显着增加。病毒回收率的增加似乎是由于潜伏病毒重新激活的诱导，而不是复制的增加，因为 5-AZC 抑制了 HSV 复制。这些数据支持甲基化在 HSV 潜伏期和重新激活中的作用。
5-Azacytidine (5-AZC) reduces cytosine methylation in DNA and has been reported to activate quiescent virus genes. Treatment of explant cultures of latently herpes simplex virus type 2 (HSV-2)-infected guinea-pig dorsal root ganglia and spinal cordsin vitrowith 5-AZC significantly enhanced the rate of HSV recovery. Both the number of isolates from ganglia (P< 0.001) and the rate of recovery (P< 0.001) were significantly increased with the addition of 50 µM-5-AZC to explant cultures. Increased virus recovery appeared to be due to the induction of reactivation of latent virus, rather than an increase in replication, since 5-AZC inhibited HSV replication. These data support a role for methylation in HSV latency and reactivation.