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Virus Infections on Prion Diseased Mice Exacerbate Inflammatory Microglial Response
Nara Lins1, Luiz Mourão1, Nonata Trévia1
1Universidade Federal do Pará, Instituto de Ciências Biológicas, Laboratório de Investigações em Neurodegeneração e Infecção no Hospital Universitário João de Barros Barreto, Belém, Brazil.
Abstract:
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 (n = 26) and ME7 (n = 29). 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.
Insights
Arbovirus infection exacerbates microglial inflammation in prion-diseased mice, altering microglia number and morphology. This interaction did not significantly worsen behavioral deficits in the prion disease model.
Area of Science:
- Neuroscience
- Immunology
- Virology
Background:
- Prion diseases, like ME7, cause progressive neurodegeneration and behavioral deficits.
- Arboviruses can cause neurological complications, and their interaction with other neurological conditions is not fully understood.
Purpose of the Study:
- To investigate the interactive effects of arbovirus (Piry) infection on prion disease (ME7) in mice.
- To assess behavioral changes and neuroinflammation in mice co-infected with Piry virus and ME7 prion strain.
Main Methods:
- Mice were intracranially injected with ME7 prion or normal brain homogenate, followed by intranasal challenge with Piry arbovirus or normal brain homogenate.
- Behavioral tests (burrowing, open field, rod bridge, inverted screen) were conducted at various time points post-injection.
- Brain tissue was analyzed for microglia (IBA1), prion protein (PrP), and viral antigens.
Main Results:
- ME7 prion infection induced progressive behavioral deficits, particularly in burrowing activity.
- Piry arbovirus infection alone did not alter microglia numbers in the CA1 region.
- In ME7-infected mice, Piry infection induced laminar-dependent changes in microglia number and morphology, suggesting exacerbated neuroinflammation.
Conclusions:
- Arbovirus infection can exacerbate microglial inflammatory responses in prion-diseased mice.
- The observed neuroinflammatory changes in co-infected mice were not directly correlated with hippocampal-dependent behavioral deficits.
- This study highlights a complex interplay between viral and prion infections in the brain.
