Hill T M, Sinden R R, Sadler J R
J Virol. 1983 Jan;45(1):241-50. doi: 10.1128/JVI.45.1.241-250.1983.
Herpes simplex virus type 1 (HSV-1) and HSV-2 disrupt host protein synthesis after viral infection. We have treated both viral types with agents which prevent transcription of the viral genome and used these treated viruses to infect induced Friend erythroleukemia cells. By measuring the changes in globin synthesis after infection, we have determined whether expression of the viral genome precedes the shutoff of host protein synthesis or whether the inhibitor molecule enters the cells as part of the virion. HSV-2-induced shutoff of host protein synthesis was insensitive to the effects of shortwave (254-nm) UV light and actinomycin D. Both of the treatments inhibited HSV-1-induced host protein shutoff. Likewise, treatment of HSV-1 with the cross-linking agent 4,5',8-trimethylpsoralen and longwave (360-nm) UV light prevented HSV-1 from inhibiting cellular protein synthesis. Treatment of HSV-2 with 4,5',8-trimethylpsoralen did not affect the ability of the virus to interfere with host protein synthesis, except at the highest doses of longwave UV light. It was determined that the highest longwave UV dosage damaged the HSV-2 virion as well as cross-linking the viral DNA. The results suggest that HSV-2 uses a virion-associated component to inhibit host protein synthesis and that HSV-1 requires the expression of the viral genome to cause cellular protein synthesis shutoff.
1型单纯疱疹病毒（HSV - 1）和2型单纯疱疹病毒（HSV - 2）在病毒感染后会破坏宿主蛋白合成。我们用能阻止病毒基因组转录的试剂处理这两种病毒类型，并使用这些处理过的病毒感染诱导型Friend红白血病细胞。通过测量感染后珠蛋白合成的变化，我们确定了病毒基因组的表达是先于宿主蛋白合成的关闭，还是抑制剂分子作为病毒粒子的一部分进入细胞。HSV - 2诱导的宿主蛋白合成关闭对短波（254纳米）紫外线和放线菌素D的作用不敏感。这两种处理都抑制了HSV - 1诱导的宿主蛋白合成关闭。同样，用交联剂4,5',8 - 三甲基补骨脂素和长波（360纳米）紫外线处理HSV - 1可防止其抑制细胞蛋白合成。用4,5',8 - 三甲基补骨脂素处理HSV - 2除了在最高剂量的长波紫外线照射下外，并不影响病毒干扰宿主蛋白合成的能力。已确定最高剂量的长波紫外线会破坏HSV - 2病毒粒子并使病毒DNA交联。结果表明，HSV - 2利用病毒粒子相关成分抑制宿主蛋白合成，而HSV - 1需要病毒基因组的表达来导致细胞蛋白合成关闭。
