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Artigo
Early and late neuropathological features of meningoencephalitis associated with Maraba virus infection
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 Par?, Amaz?nia, Brazil. Despite 30 years having passed since its isolation, little is known about the neuropathology induced by...
Autor principal: | Farias, Alexandre Maia de |
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Outros Autores: | Lima, Camila Mendes de, Freitas, Priscilla dos Santos Lieuthier, Diniz, Daniel Guerreiro, Rodrigues, Ana Paula Drummond, Quaresma, Juarez, Diniz, Cristovam Wanderley Pican?o, Diniz, Jos? Antonio Pican?o |
Grau: | Artigo |
Idioma: | eng |
Publicado em: |
Associa??o Brasileira de Divulga??o Cient?fica
2020
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Assuntos: | |
Acesso em linha: |
http://patua.iec.gov.br//handle/iec/4085 |
Resumo: |
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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 Par?, Amaz?nia, 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)-a, interferon (INF)-g, 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. |