Falser N, Bandtlow I, Rziha H J, Haus M, Wolf H
Am J Otol. 1987 Mar;8(2):136-47.
The possible role of herpesviral infections of the inner ear in suddenly appearing inner ear disturbances was investigated. Experimental pseudorabies virus (PRV, Herpes sui 1) infection of mice and swine was used as a model system. Infected mice represented the productive cycle of PRV infection (acute phase), whereas the latent phase of infection could be tested in swine. From the acutely infected mice the virus could be reisolated from perilymphatic fluid and various parts of the brain. Massive histopathologic alterations and signs of total cell damage to the organ of Corti and the vestibular organ were found. Accordingly, in all of the cells of the inner ear multiple copies of the PRV genome could be demonstrated. We therefore suggest that the disturbances of the inner ear were induced by the acute virus infection. In two latently infected swine (sixty weeks after infection), PRV could not be recovered either from the perilymphatic fluid or from a variety of different neural and extraneural tissues. However, histopathologic changes similar to those found in the acutely infected mice were observed. The presence of viral DNA could be demonstrated by in situ cytohybridization in both sensory and supportive cells of the inner ear and vestibular organ, but not in the corresponding nerve fibers, which is in contrast to the acutely infected mice. The distribution of the viral genome was further analyzed in adjacent areas of the central nervous system. An involvement of acute and latent herpes virus infection in inner ear dysfunction including sudden deafness and vestibular neuronitis in man, might be suggested from the results described. The presented animal model system, PRV-infected swine, should permit further studies on a possible role of herpetic recurrences, particularly with regard to inner ear disturbances.
研究了内耳疱疹病毒感染在突然出现的内耳功能障碍中可能发挥的作用。将实验性伪狂犬病病毒（PRV，猪疱疹病毒1型）感染小鼠和猪作为模型系统。感染的小鼠代表PRV感染的增殖周期（急性期），而感染的潜伏期可在猪身上进行检测。在急性感染的小鼠中，可从外淋巴液和大脑的各个部位重新分离出病毒。发现了大量的组织病理学改变以及柯蒂氏器和前庭器官的细胞完全受损的迹象。相应地，在内耳的所有细胞中都能证明有多个PRV基因组拷贝。因此，我们认为内耳功能障碍是由急性病毒感染引起的。在两只潜伏感染的猪（感染后60周）中，无论是从外淋巴液还是从各种不同的神经和神经外组织中都无法检测到PRV。然而，观察到了与急性感染小鼠中发现的类似的组织病理学变化。通过原位细胞杂交在内耳和前庭器官的感觉细胞和支持细胞中都能证明病毒DNA的存在，但在相应的神经纤维中则没有，这与急性感染的小鼠不同。在中枢神经系统的相邻区域进一步分析了病毒基因组的分布。从所描述的结果可能提示，急性和潜伏性疱疹病毒感染与人的内耳功能障碍（包括突发性耳聋和前庭神经炎）有关。所提出的动物模型系统，即PRV感染的猪，应该能够允许对疱疹复发的可能作用进行进一步研究，特别是关于内耳功能障碍方面。
