Mouse model of neurological complications resulting from encephalitic alphavirus infection
Open accessAbstract
Long-term neurological complications, termed sequelae, can result from viral encephalitis, which are not well understood. In human survivors, alphavirus encephalitis can cause severe neurobehavioral changes, in the most extreme cases, a schizophrenic-like syndrome. In the present study, we aimed to adapt an animal model of alphavirus infection survival to study the development of these long-term neurological complications. Upon low-dose infection of wild-type C57B/6 mice, asymptomatic and symptomatic groups were established and compared to mock-infected mice to measure general health and baseline neurological function, including the acoustic startle response and prepulse inhibition paradigm. Prepulse inhibition is a robust operational measure of sensorimotor gating, a fundamental form of information processing. Deficits in prepulse inhibition manifest as the inability to filter out extraneous sensory stimuli. Sensory gating is disrupted in schizophrenia and other mental disorders, as well as neurodegenerative diseases. Symptomatic mice developed deficits in prepulse inhibition that lasted through 6 months post infection; these deficits were absent in asymptomatic or mock-infected groups. Accompanying prepulse inhibition deficits, symptomatic animals exhibited thalamus damage as visualized with H&E staining, as well as increased GFAP expression in the posterior complex of the thalamus and dentate gyrus of the hippocampus. These histological changes and increased GFAP expression were absent in the asymptomatic and mock-infected animals, indicating that glial scarring could have contributed to the prepulse inhibition phenotype observed in the symptomatic animals. This model provides a tool to test mechanisms of and treatments for the neurological sequelae of viral encephalitis and begins to delineate potential explanations for the development of such sequelae post infection.
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We did not detect clinical symptoms in inoculated WT mice.
“We did not detect clinical symptoms in inoculated WT mice, as previously described (Ronca et al., 2017).”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Ronca et al., 2017
The Results (General Health Assessment) report clinical symptoms in 3 of 10 inoculated wild-type mice, including ruffled fur, hunched back, and reduced activity. Although the other 7 mice were asymptomatic, the paper does not describe an absence of clinical symptoms in inoculated wild-type mice as a group. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredViral infections may play a role in developing and progressing neurodegenerative disorders, particularly Alzheimer's disease.
“suggesting a potential role in developing and progressing neurodegenerative disorders, particularly AD (Bantle et al., 2019; Piekut et al., 2022; Ronca et al., 2017).”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Ronca et al., 2017
The Conclusion says viral infections can lead to or exacerbate neurological disorders. The Introduction and Discussion link a sensorimotor-gating deficit seen in infected mice to deficits associated with Alzheimer’s disease, but they do not say that infection contributes to the development or progression of Alzheimer’s disease specifically. Page numbers were not available in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredViral infections such as Herpes simplex encephalitis, Epstein-Barr virus, Eastern Equine Encephalitis virus, Western Equine Encephalitis virus, and Venezuelan Equine Encephalitis Virus correlate with negative neurological consequences even after the acute phase.
“Several studies have shown that viral infections, such as Herpes simplex encephalitis, Epstein-Barr virus, Eastern Equine Encephalitis virus (EEEV), Western Equine Encephalitis virus (WEEV), and Venezuelan Equine Encephalitis Virus (VEEV), correlate with negative neurological consequences even after the acute phase”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Ronca et al., 2017
The Introduction (page unavailable) identifies VEEV, EEEV, and WEEV as associated with neurological sequelae in survivors, including symptoms after recovery. It does not address herpes simplex encephalitis or Epstein–Barr virus; searches for both returned no relevant passage. (LLM, conf=0.90)
Experimental — accuracy not yet measuredIn a mouse model of VEEV encephalitis, mice display behavioral and neuropathological phenotypes associated with schizophrenia, Alzheimer's disease, and autism spectrum disorders.
“In a mouse model of VEEV encephalitis, mice displayed behavioral and neuropathological phenotypes associated with several neurological disorders, including schizophrenia, Alzheimer's disease (AD), and autism spectrum disorders (Ronca et al., 2017).”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Ronca et al., 2017
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- Authors
- Ronca, S. E., Smith, J., Koma, T., Miller, M. M., Yun, N., Dineley, K. T., & Paessler, S.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Corresponding author
- Paessler, Slobodan
- Venue
- Frontiers in Microbiology
- Publisher
- Frontiers Media SA
- Published
- 2017-02-07
- Volume
- 8
- Pages
- 188-188
- ISSN
- 1664-302X (ISSN-L)
- PMC
- PMC5293790
- OpenAlex
- W2587380678
- Cited by
- 22
- References
- 76
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 4 · 2023: 2 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 1
- FWCI
- 0.84
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Microbiology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institutes of Health (TL1TR001440)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Infectious Diseases › Infectious Encephalopathies and Encephalitis
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Mosquito-borne diseases and control
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- neurological sequelae, prepulse inhibition, sensorimotor gating, glial scar, GFAP expression, hippocampus, dentate gyrus, acoustic startle response, C57BL/6 mice, viral encephalitis, animal models
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