Theiler's Virus
Theiler's Virus - Related Videos
05:33
A Model for Epilepsy of Infectious Etiology using Theiler's Murine Encephalomyelitis Virus
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Cited by 7 •
2022
Intracerebral infection with the Theiler's murine encephalomyelitis virus (TMEV) in C57BL/6 mice replicates many of the early and chronic clinical symptoms of viral encephalitis and subsequent epilepsy in human patients. This paper describes the virus infection, symptoms, and histopathology of the TMEV model.
00:50
What are Viruses?
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2019
Overview A virus is a microscopic infectious particle that consists of an RNA or DNA genome enclosed in a protein shell. It is not able to reproduce on its own: it can only make more viruses by entering a cell and using its cellular machinery. When a virus infects a host cell, it removes its protein coat and directs the host’s machinery to transcribe and translate its genetic material. The hijacked cell assembles the replicated components into thousands of viral progeny, which can rupture and...
10:35
Vector Competence Analyses on Aedes aegypti Mosquitoes using Zika Virus
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Cited by 3 •
2020
The presented protocol can determine the vector competence of Aedes aegypti mosquito populations for a given virus, such as Zika, in a containment setting.
12:52
Propagation of Homalodisca coagulata virus-01 via Homalodisca vitripennis Cell Culture
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Cited by 4 •
2014
Here we present a protocol to propagate Homalodisca vitripennis cells and HoCV-1 in vitro. Medium was removed from HoCV-1 positive cultures and RNA extracted every 24 hr for 168 hr. Cell survivability was quantified by trypan blue staining. Whole virus particles were extracted post-infection. Extracted RNA was quantified by qRT-PCR.
18:10
Isolation of Fidelity Variants of RNA Viruses and Characterization of Virus Mutation Frequency
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Cited by 40 •
2011
The present article describes the steps required to isolate and characterize RNA polymerase fidelity variants of RNA viruses and how to use mutation frequency data to confirm fidelity changes in tissue culture.
FAQs
Strain-dependent disease courses help separate acute neuronal injury from chronic inflammatory damage. Some strains primarily produce early damage to neurons, whereas others support persistence in glial cells and white-matter regions. Comparing these outcomes allows neuroscience researchers to examine how viral behavior influences tissue vulnerability, immune activation, and the development of demyelinating pathology.
Persistence maintains a continuing stimulus within neural tissue rather than limiting disease to an acute infection. When virus remains associated with glial cells and white-matter regions, immune activity can contribute to loss of myelin. This relationship enables researchers to investigate how an ongoing viral presence may sustain inflammation and promote chronic central nervous system injury.
Microglia and T cells provide complementary perspectives on neuroinflammation. Microglia represent immune activity within the nervous system, while T cells reflect an adaptive immune response that can interact with infected or damaged neural tissue. Studying both populations helps clarify how cellular immunity contributes to demyelination, axonal damage, and persistent inflammatory changes.
The model connects viral persistence with immune-mediated injury in central nervous system white matter. Researchers use that relationship to examine demyelination, neuroinflammation, and axonal damage in a controlled experimental setting. Its value lies in linking an initiating infection with chronic tissue changes that resemble important features of multiple-sclerosis-like pathology.
Theiler’s virus supports investigation of several connected outcomes, including acute neuronal injury, persistent glial infection, white-matter inflammation, demyelination, and axonal damage. Examining these processes together helps researchers determine how infection and host immune responses influence neural tissue over time, rather than treating viral presence as an isolated event.
Because the model brings together viral persistence, microglial activity, T-cell responses, demyelination, and axonal injury, it provides a framework for evaluating strategies aimed at chronic neuroinflammation. Researchers can use the resulting pathology to ask whether a potential therapy alters immune-mediated damage or protects neural tissue during persistent inflammatory disease.