Zucker M L, Prusoff W H
Yale University School of Medicine, New Haven, CT 06510.
Biochem Pharmacol. 1987 Oct 15;36(20):3471-6. doi: 10.1016/0006-2952(87)90328-5.
First generation progeny herpes simplex type 1 (HSV-1) virions grown in the presence of 5-iodo-2'-deoxyuridine (IdUrd) were irradiated with either 254 or 302 nm ultraviolet (u.v.) light. The kinetics of virus inactivation revealed decreased sensitivity of IdUrd-substituted virions to irradiation with 302 nm light under all conditions examined, and with 254 nm u.v. light when substituted and control virions were irradiated at equal particle concentrations. Comparison of virus survival after irradiation measured in Vero or Xeroderma Pigmentosum (complementation group A) cells indicated that cellular repair of ultraviolet-induced lesions was not a significant factor in the observed decrease in u.v. sensitivity. IdUrd substitution altered neither the formation of ultraviolet-induced thymidine photoproducts nor the ability of irradiated virions to express delayed early viral enzymes (thymidine kinase, DNA polymerase). It is suggested that nucleocapsid proteins or the highly ordered structure of IdUrd-substituted virions play a key role in u.v. desensitization, either by the formation of non-lethal photoproducts or by the prevention of the formation of DNA-uracilyl free radicals.
在5-碘-2'-脱氧尿苷（IdUrd）存在下培养的第一代单纯疱疹病毒1型（HSV-1）病毒粒子，用254或302纳米紫外线（uv）照射。病毒灭活动力学显示，在所有检测条件下，IdUrd取代的病毒粒子对302纳米光照射的敏感性降低，当取代病毒粒子和对照病毒粒子以相同粒子浓度照射时，对254纳米紫外线照射的敏感性也降低。在Vero细胞或着色性干皮病（互补组A）细胞中测量照射后病毒存活情况的比较表明，紫外线诱导损伤的细胞修复不是观察到的紫外线敏感性降低的重要因素。IdUrd取代既不改变紫外线诱导的胸苷光产物的形成，也不改变照射病毒粒子表达延迟早期病毒酶（胸苷激酶、DNA聚合酶）的能力。有人提出，核衣壳蛋白或IdUrd取代病毒粒子的高度有序结构在紫外线脱敏中起关键作用，要么通过形成非致死性光产物，要么通过防止DNA-尿嘧啶自由基的形成。
