Lycke E
Department of Clinical Virology, University of Göteborg, Sweden.
Scand J Infect Dis Suppl. 1990;69:113-9.
Latent reactivateable herpes simplex virus (HSV) infections of sensory neurons of peripheral ganglia are most plausibly the source of clinical herpetic recurrences. The establishment of latency is the result of a concert of both viral and cellular factors such as the neuroinvasiveness of the virus, the relative density of receptors binding virus to the nerve cell plasma membrane, the permissiveness of the infection, including the axonal transport of the viral nucleocapsids, and the restriction of virus replication. Several hypotheses have been presented suggesting various mechanisms for the restriction of the HSV infection of the neuron. Thus, for instance the the importance of thymidine kinase negative mutants, hypermethylation of viral DNA and the existence of latency-associated viral genes have been discussed. Activation of the latent infection to a virus-producing lytic infection by means of superinfection with a replication-incompetent mutant is probably a result of genetic complementation. Reactivation by means of superinfection with replication-competent virus seems dependent upon the multiplicity of the superinfecting virus and more than one copy of the virus genome is required for the initiation of the reactivating process. These observations would be consistent with the overcoming of a cellularly controlled restriction of the latent infection. The cellular control of latency which can be impaired mechanically and chemically seems particularly important for the maintenance of latent HSV infection. However, recent observations indicate that reactivation of latent HSV infection is also associated with the expression of a latency-related viral gene (LAT), whereas establishment of the latency apparently is influenced by other properties determined by the genome of the virus, as well as by the capacity of the cell to restrict the lytic infection.
外周神经节感觉神经元的潜伏性可再激活单纯疱疹病毒（HSV）感染很可能是临床疱疹复发的根源。潜伏状态的建立是病毒和细胞因素共同作用的结果，这些因素包括病毒的神经侵袭性、病毒与神经细胞质膜结合受体的相对密度、感染的允许性，包括病毒核衣壳的轴突运输，以及病毒复制的限制。已经提出了几种假说，暗示了限制神经元HSV感染的各种机制。例如，已经讨论了胸苷激酶阴性突变体的重要性、病毒DNA的高甲基化以及潜伏相关病毒基因的存在。通过用复制缺陷型突变体进行超感染将潜伏感染激活为产生病毒的裂解感染，可能是基因互补的结果。通过用具有复制能力的病毒进行超感染来重新激活似乎取决于超感染病毒的复数性，并且重新激活过程的启动需要不止一份病毒基因组。这些观察结果与克服潜伏感染的细胞控制限制是一致的。潜伏的细胞控制可以通过机械和化学方式受损，这对于维持潜伏性HSV感染似乎尤为重要。然而，最近的观察表明，潜伏性HSV感染的重新激活也与一种潜伏相关病毒基因（LAT）的表达有关，而潜伏状态的建立显然受到病毒基因组决定的其他特性以及细胞限制裂解感染能力的影响。
