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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 3974648, 12 pages
Research Article

Virus Infections on Prion Diseased Mice Exacerbate Inflammatory Microglial Response

1Universidade Federal do Pará, Instituto de Ciências Biológicas, Laboratório de Investigações em Neurodegeneração e Infecção no Hospital Universitário João de Barros Barreto, Belém, Brazil
2Instituto Evandro Chagas, Laboratório de Microscopia Eletrônica and Departamento de Arbovirologia e Febres Hemorrágicas Virais, Belém, Brazil

Received 4 August 2016; Revised 22 September 2016; Accepted 27 September 2016

Academic Editor: Michael D. Coleman

Copyright © 2016 Nara Lins et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We investigated possible interaction between an arbovirus infection and the ME7 induced mice prion disease. C57BL/6, females, 6-week-old, were submitted to a bilateral intrahippocampal injection of ME7 prion strain (ME7) or normal brain homogenate (NBH). After injections, animals were organized into two groups: NBH () and ME7 (). At 15th week after injections (wpi), animals were challenged intranasally with a suspension of Piry arbovirus 0.001% or with NBH. Behavioral changes in ME7 animals appeared in burrowing activity at 14 wpi. Hyperactivity on open field test, errors on rod bridge, and time reduction in inverted screen were detected at 15th, 19th, and 20th wpi respectively. Burrowing was more sensitive to earlier hippocampus dysfunction. However, Piry-infection did not significantly affect the already ongoing burrowing decline in the ME7-treated mice. After behavioral tests, brains were processed for IBA1, protease-resistant form of PrP, and Piry virus antigens. Although virus infection in isolation did not change the number of microglia in CA1, virus infection in prion diseased mice (at 17th wpi) induced changes in number and morphology of microglia in a laminar-dependent way. We suggest that virus infection exacerbates microglial inflammatory response to a greater degree in prion-infected mice, and this is not necessarily correlated with hippocampal-dependent behavioral deficits.