Steiner I
Department of Neurology, Hadassah University Hospital, Jerusalem, Israel.
Immunol Rev. 1996 Aug;152:157-73. doi: 10.1111/j.1600-065x.1996.tb00915.x.
The neurotropic herpes viruses, HSV-1, HSV-2 and VZV, colonize and establish latent infection in human peripheral sensory ganglia. Recurrent diseases due to reactivation of these viral pathogens can take place despite an effective immune response. Molecular, cellular, physiological and immune mechanisms work in concert to enable the establishment of latency, the maintenance of the latent state for the entire life of the host, and the reactivation infection. Although all three viruses belong to the same family and establish latent infection in the same tissue, the clinical pattern of their reactivation is quite different. This review covers current knowledge of the basis of these infections, and offers a theory explaining the basis of HSV-1 latent infection and the differences of the disorders caused by HSV-1 and VZV reactivation in humans.
嗜神经疱疹病毒,即单纯疱疹病毒1型(HSV-1)、单纯疱疹病毒2型(HSV-2)和水痘-带状疱疹病毒(VZV),在人类外周感觉神经节中定植并建立潜伏感染。尽管有有效的免疫反应,这些病毒病原体重新激活仍可导致复发性疾病。分子、细胞、生理和免疫机制协同作用,以实现潜伏感染的建立、在宿主整个生命周期中维持潜伏状态以及重新激活感染。虽然这三种病毒属于同一科,并在同一组织中建立潜伏感染,但其重新激活的临床模式却大不相同。本综述涵盖了这些感染基础的当前知识,并提出了一种理论,解释HSV-1潜伏感染的基础以及HSV-1和VZV在人类中重新激活所导致疾病的差异。