Klein R J
Am J Med. 1982 Jul 20;73(1A):138-42. doi: 10.1016/0002-9343(82)90079-1.
Acyclovir can prevent the establishment of latent herpes simplex virus (HSV) in sensory ganglia by early treatment of the primary infection in experimental animals. A delayed treatment may reduce the number of neurons that eventually become latently infected. Acyclovir can prevent virus reactivation in explant cultures of latently infected ganglia, experimentally induced recurrences of latently infected animals, and immunosuppressed patients. This effect is dependent on the continuous presence of the drug in the explant culture medium or organism. The treatment of recurrent lesions with acyclovir reduces the severity of the episode and may also prevent reinfection of ganglia, if this should be common in the maintenance of latency. It might be possible to eradicate a latent HSV, if conditions were created in which drugs such as acyclovir, activated by the virus-induced thymidine kinase, could interact with the enzyme before the assembly of mature virions.
阿昔洛韦通过早期治疗实验动物的原发性感染，可预防单纯疱疹病毒（HSV）在感觉神经节中建立潜伏感染。延迟治疗可能会减少最终发生潜伏感染的神经元数量。阿昔洛韦可预防潜伏感染神经节的外植体培养物中病毒的重新激活、潜伏感染动物实验诱导的复发以及免疫抑制患者的复发。这种作用取决于药物在体外培养介质或生物体内的持续存在。用阿昔洛韦治疗复发性损害可减轻发作的严重程度，并且如果在潜伏状态维持过程中这种情况常见的话，还可能预防神经节的再次感染。如果创造条件使病毒诱导的胸苷激酶激活的阿昔洛韦等药物在成熟病毒体组装之前就能与该酶相互作用，那么有可能根除潜伏的HSV。
