Diniz José Antonio Picanço, Dos Santos Zaire Alves, Braga Marcio Augusto Galvão, Dias Adila Liliane Barros, da Silva Daisy Elaine Andrade, de Almeida Medeiros Daniele Barbosa, de Souza Barros Vera Lucia Reis, Chiang Jannifer Oliveira, de Freitas Zoghbi Kendra Eyllen, Quaresma Juarez Antônio Simões, Takiya Christina Maeda, Moura Neto Vivaldo, de Souza Wanderley, da Costa Vasconcelos Pedro Fernando, Diniz Cristovam Wanderley Picanço
Instituto Evandro Chagas, Belém, Brazil.
PLoS One. 2008 Mar 5;3(3):e1733. doi: 10.1371/journal.pone.0001733.
In previous reports we proposed a new genus for Rhabdoviridae and described neurotropic preference and gross neuropathology in newborn albino Swiss mice after Curionopolis and Itacaiunas infections. In the present report a time-course study of experimental encephalitis induced by Itacaiunas and Curionopolis virus was conducted both in vivo and in vitro to investigate cellular targets and the sequence of neuroinvasion. We also investigate, after intranasal inoculation, clinical signs, histopathology and apoptosis in correlation with viral immunolabeling at different time points. Curionopolis and Itacaiunas viral antigens were first detected in the parenchyma of olfactory pathways at 2 and 3 days post-inoculation (dpi) and the first clinical signs were observed at 4 and 8 dpi, respectively. After Curionopolis infection, the mortality rate was 100% between 5 and 6 dpi, and 35% between 8 and 15 dpi after Itacaiunas infection. We identified CNS mice cell types both in vivo and in vitro and the temporal sequence of neuroanatomical olfactory areas infected by Itacaiunas and Curionopolis virus. Distinct virulences were reflected in the neuropathological changes including TUNEL immunolabeling and cytopathic effects, more intense and precocious after intracerebral or in vitro inoculations of Curionopolis than after Itacaiunas virus. In vitro studies revealed neuronal but not astrocyte or microglial cytopathic effects at 2 dpi, with monolayer destruction occurring at 5 and 7 dpi with Curionopolis and Itacaiunas virus, respectively. Ultrastructural changes included virus budding associated with interstitial and perivascular edema, endothelial hypertrophy, a reduced and/or collapsed small vessel luminal area, thickening of the capillary basement membrane, and presence of phagocytosed apoptotic bodies. Glial cells with viral budding similar to oligodendrocytes were infected with Itacaiunas virus but not with Curionopolis virus. Thus, Curionopolis and Itacaiunas viruses share many pathological and clinical features present in other rhabdoviruses but distinct virulence and glial targets in newborn albino Swiss mice brain.
在之前的报告中,我们为弹状病毒科提出了一个新属,并描述了库里奥诺波利斯病毒和伊塔卡尤纳斯病毒感染新生白化瑞士小鼠后的嗜神经性偏好和大体神经病理学变化。在本报告中,我们对伊塔卡尤纳斯病毒和库里奥诺波利斯病毒诱导的实验性脑炎进行了体内和体外的时间进程研究,以调查细胞靶点和神经侵袭的顺序。我们还在鼻内接种后,研究了不同时间点的临床症状、组织病理学和细胞凋亡与病毒免疫标记的相关性。库里奥诺波利斯病毒和伊塔卡尤纳斯病毒抗原分别在接种后2天和3天首次在嗅觉通路实质中检测到,首次临床症状分别在接种后4天和8天观察到。库里奥诺波利斯病毒感染后,在接种后5至6天死亡率为100%,伊塔卡尤纳斯病毒感染后在接种后8至15天死亡率为35%。我们在体内和体外鉴定了中枢神经系统小鼠细胞类型以及伊塔卡尤纳斯病毒和库里奥诺波利斯病毒感染的神经解剖学嗅觉区域的时间顺序。不同的毒力反映在神经病理学变化中,包括TUNEL免疫标记和细胞病变效应,库里奥诺波利斯病毒脑内或体外接种后比伊塔卡尤纳斯病毒更强烈和早熟。体外研究显示,接种后2天神经元出现细胞病变效应,但星形胶质细胞或小胶质细胞未出现,库里奥诺波利斯病毒和伊塔卡尤纳斯病毒分别在接种后5天和7天出现单层破坏。超微结构变化包括与间质和血管周围水肿、内皮肥大、小血管腔面积减小和/或塌陷、毛细血管基底膜增厚以及吞噬的凋亡小体存在相关的病毒出芽。感染伊塔卡尤纳斯病毒而非库里奥诺波利斯病毒的神经胶质细胞出现类似于少突胶质细胞的病毒出芽。因此,库里奥诺波利斯病毒和伊塔卡尤纳斯病毒具有其他弹状病毒共有的许多病理和临床特征,但在新生白化瑞士小鼠脑中具有不同的毒力和神经胶质细胞靶点。