Department of DCCA and DCCRA, Veterinary School, Laboratory of Virology, Clovis Pestana Street, Araçatuba, 16,050-680, Brazil.
Diagn Pathol. 2010 Sep 10;5:57. doi: 10.1186/1746-1596-5-57.
Meningoencephalitis by Herpesvirus type 5 (BoHV-5) in cattle has some features that are similar to those of herpetic encephalitis in humans and other animal species. Human Herpesvirus 3 (commonly known as Varicella-zoster virus 1), herpes simplex viruses (HSV), and equid Herpesvirus 1 (EHV-1) induce an intense inflammatory, vascular and cellular response. In spite of the many reports describing the histological lesions associated with natural and experimental infections, the immunopathological mechanisms for the development of neurological disorder have not been established. A total of twenty calf brains were selected from the Veterinary School, University of São Paulo State, Araçatuba, Brazil, after confirmation of BoHV-5 infection by virus isolation as well as by a molecular approach. The first part of the study characterized the microscopic lesions associated with the brain areas in the central nervous system (CNS) that tested positive in a viral US9 gene hybridization assay. The frontal cortex (Fc), parietal cortex (Pc), thalamus (T) and mesencephalon (M) were studied. Secondly, distinct pathogenesis mechanisms that take place in acute cases were investigated by an immunohistochemistry assay. This study found the frontal cortex to be the main region where intense oxidative stress phenomena (AOP-1) and synaptic protein expression (SNAP-25) were closely related to inflammatory cuffs, satellitosis and gliosis, which represent the most frequently observed neurological lesions. Moreover, MMP-9 expression was shown to be localized in the leptomeninges, in the parenchyma and around mononuclear infiltrates (p < 0.0001). These data open a new perspective in understanding the role of the AOP-1, MMP-9 and SNAP-25 proteins in mediating BoHV-5 pathogenesis and the strategies of host-virus interaction in order to invade the CNS.
牛的 5 型疱疹病毒（BoHV-5）引起的脑膜脑炎在某些特征上与人类和其他动物的疱疹脑炎相似。人类疱疹病毒 3（俗称水痘-带状疱疹病毒 1）、单纯疱疹病毒（HSV）和马疱疹病毒 1（EHV-1）会引起强烈的炎症、血管和细胞反应。尽管有许多报道描述了与自然和实验感染相关的组织学病变，但尚未确定导致神经紊乱的免疫病理机制。巴西阿拉萨图巴州立大学兽医学院共从 20 头小牛脑中选择了脑组织，这些小牛脑通过病毒分离以及分子方法确认感染了 BoHV-5。研究的第一部分描述了与中枢神经系统（CNS）中病毒 US9 基因杂交检测呈阳性的脑区相关的微观病变。研究了额叶皮质（Fc）、顶叶皮质（Pc）、丘脑（T）和中脑（M）。其次，通过免疫组织化学检测研究了急性病例中发生的不同发病机制。这项研究发现，额叶皮质是强烈氧化应激现象（AOP-1）和突触蛋白表达（SNAP-25）与炎症袖套、卫星现象和神经胶质增生密切相关的主要区域，这是最常观察到的神经病变。此外，MMP-9 表达被证明定位于软脑膜、实质和单核细胞浸润周围（p < 0.0001）。这些数据为理解 AOP-1、MMP-9 和 SNAP-25 蛋白在介导 BoHV-5 发病机制以及宿主-病毒相互作用策略以入侵中枢神经系统方面的作用开辟了新的视角。
