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与马雅罗病毒感染相关的脑膜脑炎的早期和晚期神经病理学特征。

Early and late neuropathological features of meningoencephalitis associated with Maraba virus infection.

机构信息

Laboratório de Microscopia Eletrônica, Instituto Evandro Chagas, Belém, PA, Brasil.

Laboratório de Neurodegeneração e Infecção, Instituto de Ciências Biológicas, Hospital Universitário João Barros Barreto, Universidade Federal do Pará, Belém, PA, Brasil.

出版信息

Braz J Med Biol Res. 2020 Mar 31;53(4):e8604. doi: 10.1590/1414-431X20208604. eCollection 2020.

DOI:10.1590/1414-431X20208604
PMID:32294697
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7162580/
Abstract

Maraba virus is a member of the genus Vesiculovirus of the Rhabdoviridae family that was isolated in 1983 from sandflies captured in the municipality of Maraba, state of Pará, Amazônia, Brazil. Despite 30 years having passed since its isolation, little is known about the neuropathology induced by the Maraba virus. Accordingly, in this study the histopathological features, inflammatory glial changes, cytokine concentrations, and nitric oxide activity in the encephalon of adult mice subjected to Maraba virus nostril infection were evaluated. The results showed that 6 days after intranasal inoculation, severe neuropathological-associated disease signs appeared, including edema, necrosis and pyknosis of neurons, generalized congestion of encephalic vessels, and intra- and perivascular meningeal lymphocytic infiltrates in several brain regions. Immunolabeling of viral antigens was observed in almost all central nervous system (CNS) areas and this was associated with intense microglial activation and astrogliosis. Compared to control animals, infected mice showed significant increases in interleukin (IL)-6, tumor necrosis factor (TNF)-α, interferon (INF)-γ, MCP-1, nitric oxide, and encephalic cytokine levels. We suggest that an exacerbated inflammatory response in several regions of the CNS of adult BALB/c mice might be responsible for their deaths.

摘要

马拉巴病毒是弹状病毒科水疱病毒属的一个成员,于 1983 年在巴西帕拉州马拉巴市捕获的沙蝇中分离出来。尽管自分离以来已经过去了 30 年,但对马拉巴病毒引起的神经病理学知之甚少。因此,在这项研究中,评估了经鼻腔感染马拉巴病毒的成年小鼠脑组织的组织病理学特征、炎症性神经胶质变化、细胞因子浓度和一氧化氮活性。结果表明,鼻内接种 6 天后,出现严重的与神经病理学相关的疾病迹象,包括神经元水肿、坏死和固缩,大脑血管广泛充血,以及几个脑区的血管内和血管周围脑膜淋巴细胞浸润。在几乎所有中枢神经系统(CNS)区域都观察到了病毒抗原的免疫标记,这与强烈的小胶质细胞激活和星形胶质细胞增生有关。与对照动物相比,感染小鼠的白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α、干扰素(INF)-γ、MCP-1、一氧化氮和大脑细胞因子水平显著增加。我们认为,成年 BALB/c 小鼠中枢神经系统几个区域的炎症反应加剧可能是导致其死亡的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/7476c689d8c5/1414-431X-bjmbr-53-4-e8604-gf007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/63a188305bfe/1414-431X-bjmbr-53-4-e8604-gf001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/6c46a4ef47fe/1414-431X-bjmbr-53-4-e8604-gf002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/64a22b09eb4a/1414-431X-bjmbr-53-4-e8604-gf003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/e3d9c14a0031/1414-431X-bjmbr-53-4-e8604-gf004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/1a65e20c7f64/1414-431X-bjmbr-53-4-e8604-gf005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/725207a96181/1414-431X-bjmbr-53-4-e8604-gf006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/7476c689d8c5/1414-431X-bjmbr-53-4-e8604-gf007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/63a188305bfe/1414-431X-bjmbr-53-4-e8604-gf001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/6c46a4ef47fe/1414-431X-bjmbr-53-4-e8604-gf002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/64a22b09eb4a/1414-431X-bjmbr-53-4-e8604-gf003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/e3d9c14a0031/1414-431X-bjmbr-53-4-e8604-gf004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/1a65e20c7f64/1414-431X-bjmbr-53-4-e8604-gf005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/725207a96181/1414-431X-bjmbr-53-4-e8604-gf006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fea/7162580/7476c689d8c5/1414-431X-bjmbr-53-4-e8604-gf007.jpg

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