Abas O M, Anwar Sh, Badr Y, Abd-Ellatieff H, Saleh A G, Nayel M, Rahman A Abd-El, Fukushi H, Yanai T
Laboratory of Veterinary Microbiology, Faculty of Applied Biological Sciences, Gifu University, 1-1 Yanagido, Gifu, Japan; Department of Animal Medicine, Faculty of Veterinary Medicine, Alexandria University, Alexandria, Egypt.
Department of Pathology, Faculty of Veterinary Medicine, Beni-Suef University, Beni-Suef, Egypt; Neuroscience Laboratory, CHU Research Center, Faculty of Medicine, Laval University, Quebec City, Canada.
J Comp Pathol. 2019 Jul;170:91-100. doi: 10.1016/j.jcpa.2019.06.002. Epub 2019 Jul 13.
The neuropathogenesis of equine herpesvirus 9 (EHV-9), a neurotropic herpesvirus, and its mutant clone (SP21) was studied experimentally in a hamster model. EHV-9-infected hamsters showed clinical signs of infection at 3 days post infection (dpi), while infection with SP21 resulted in clinical signs at 4 dpi. Clinical signs were more severe in the EHV-9-infected group than in the SP21-infected group. There was a significant difference in the time of anterograde transmission of EHV-9 and SP21 inside the brain. Viraemia was detected in the EHV-9-infected group at 4-5 dpi, while no viraemia was detected in the SP21-infected group. The serum concentration of tumour necrosis factor-α was significantly higher in EHV-9-infected animals than in those infected by SP21 group at 4-5 dpi, but there was no difference in the serum concentration of interferon-γ. The spatiotemporal profiles of viral replication and virus-associated histopathology were remarkably similar, were high in the olfactory bulb and cerebral hemispheres, and decreased progressively towards the medulla oblongata. The mean group scores of the histopathological changes for the entire brain were significantly higher in the EHV-9 group than in the SP21 group at all time points, starting from 3 dpi. These results suggest that the gene products of the open reading frame (ORF)19 and ORF14 play essential roles in the neuropathogenesis of EHV-9, as the two point-mutations detected in SP21 significantly altered the neuropathogenesis of the virus.
马疱疹病毒9型（EHV - 9）是一种嗜神经性疱疹病毒，对其及其突变克隆体（SP21）的神经发病机制在仓鼠模型中进行了实验研究。感染EHV - 9的仓鼠在感染后3天（dpi）出现感染的临床症状，而感染SP21的仓鼠在4 dpi出现临床症状。EHV - 9感染组的临床症状比SP21感染组更严重。EHV - 9和SP21在脑内顺行传播的时间存在显著差异。在EHV - 9感染组4 - 5 dpi检测到病毒血症，而SP21感染组未检测到病毒血症。在4 - 5 dpi时，EHV - 9感染动物的血清肿瘤坏死因子-α浓度显著高于SP21感染组，但血清干扰素-γ浓度无差异。病毒复制和病毒相关组织病理学的时空分布非常相似，在嗅球和大脑半球中含量较高，并向延髓逐渐降低。从3 dpi开始的所有时间点，EHV - 9组整个大脑组织病理学变化的平均组评分均显著高于SP21组。这些结果表明，开放阅读框（ORF）19和ORF14的基因产物在EHV - 9的神经发病机制中起重要作用，因为在SP21中检测到的两个点突变显著改变了病毒的神经发病机制。
