LATENT VIRUS INFECTION AND REACTIVATION

单纯疱疹病毒(HSV)的潜伏期被很好地描述为 人类神经系统的感染，通常是感觉神经节神经元。 潜伏的单纯疱疹病毒感染是反复感染单纯疱疹病毒的底物 也可能是其他疾病。建立单纯疱疹病毒感染的机制 神经元感染的潜伏期和重新激活在很大程度上是未知的。在……里面 为了建立HSV潜伏期，很可能是裂解的HSV级联 需要减少。假设这一点可以部分实现。 通过神经元特异的转录调节因子。类似的因素可能会 参与潜伏感染神经元的重新激活过程，因为 许多神经元不太可能通过重新激活而被破坏，尽管 传染性病毒被合成。将在#年调查HSV延迟 新生小鼠，在神经切除和神经节移植后，情况 这有望改变神经元的转录机制。 HSV RNA转录将通过原位杂交和斑点杂交进行研究。 同样，在细胞转录调控中具有潜在重要性 溶血性感染的控制将通过这些技术进行研究。新开 开发的神经节移植技术将被用于 从宿主角度探讨单纯疱疹病毒潜伏期的分子发病机制 可能干扰血管内皮细胞生长的因素和药物 建立潜伏期。最后，我们将评估可能的非神经性 至少部分HSV潜伏期的部位及HSV感染对机体的影响 神经节神经元功能在神经肽表达研究中的应用。单纯疱疹病毒 感染明显改变了体内的神经元功能，尽管这已经是 不同寻常的研究。 这些研究将提供对分子和细胞的洞察 HSV潜伏期的基础，以及对神经元改变的理解 由于单纯疱疹病毒感染而产生的功能。

Herpes simplex virus (HSV) latency has been well characterized as an infection of the human nervous system, usually of sensory ganglion neurons. Latent HSV infections are the substrate of recurrent HSV infections and possibly other illnesses as well. Mechanisms for the establishment of HSV latency and reactivation of infection in neurons are largely unknown. In order to establish HSV latency, it is likely that the lytic HSV cascade need be diminished. It is hypothesized that this may be achieved partially by neuron-specific transcription regulators. Similar factors are likely to be involved in the reactivation process in latently infected neurons, since it is improbable that many neurons are destroyed by reactivation, although infectious virus is synthesized. HSV latency will be investigated in newborn mice, after neurectomy and in ganglion transplants, situations which are expected to alter neuronal transcription mechanisms. HSV RNA transcription will be studied by in situ and blot hybridization. Similarly, cellular transcriptional regulators of potential importance in control of the lytic infection will be studied by these techniques. Newly developed ganglion transplantation techniques will be utilized to investigate the molecular pathogenesis of HSV latency in terms of host factors and pharmacological agents that may interfere with the establishment of latency. Lastly, we will evaluate the likely non-neuronal site of at least some HSV latency and the effect of HSV infection on ganglion neuron function in studies of neuropeptide expression. HSV infection clearly alters in vivo neuronal function, although this has been uncommonly studied. These investigations will provide insights to the molecular and cellular basis of HSV latency, as well as an understanding altered neuronal functioning which results from HSV infection.