Cook M L, Thompson R L, Stevens J G
Virology. 1986 Nov;155(1):293-6. doi: 10.1016/0042-6822(86)90192-3.
When the replicative defect in the HSV-1 temperature sensitive mutant tsI was repaired, the agent derived (RI-1) was found to possess an additional temperature sensitive lesion limiting its reactivation from the latent state. Thus, when spinal ganglia from latently infected mice were scored for reactivation by cocultivating them with indicator cells in vitro, significantly more were found to be positive at 31 degrees than at 38.5 degrees. To assess a possible relationship between reactivation and replication in neurons, the replication of RI-1 in murine C1300 neuroblastoma cells was studied. In these cells, RI-1 was severely restricted, and viral replication was delayed at 38.5 degrees. Serial passage of RI-1 in neuroblastoma cells at the restrictive temperature resulted in selection of an agent which gained both the capacity to replicate efficiently in neuroblastoma cells and reactivate from the latent state at 38.5 degrees. However, the replication pattern of this neuron adapted virus in mouse embryo fibroblasts remained unchanged from the parental RI-1. Taken together, these results indicate that RI-1 possesses a neuron specific temperature sensitive replicative lesion which is also manifest during reactivation from the latent state.
当单纯疱疹病毒1型（HSV-1）温度敏感突变体tsI的复制缺陷得到修复时，发现衍生制剂（RI-1）存在另一种温度敏感损伤，限制了其从潜伏状态的重新激活。因此，当通过体外与指示细胞共培养来对潜伏感染小鼠的脊髓神经节进行重新激活评分时，发现31℃时呈阳性的神经节明显多于38.5℃时。为了评估神经元中重新激活与复制之间的可能关系，研究了RI-1在鼠C1300神经母细胞瘤细胞中的复制。在这些细胞中，RI-1受到严重限制，并且在38.5℃时病毒复制延迟。在限制温度下，RI-1在神经母细胞瘤细胞中连续传代，导致选择出一种制剂，该制剂获得了在神经母细胞瘤细胞中高效复制以及在38.5℃时从潜伏状态重新激活的能力。然而，这种适应神经元的病毒在小鼠胚胎成纤维细胞中的复制模式与亲本RI-1相比没有变化。综上所述，这些结果表明RI-1具有神经元特异性温度敏感复制损伤，这种损伤在从潜伏状态重新激活期间也会表现出来。
