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A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Acute hepatitis associated with mouse leukemia. V. The neurotropic properties of the causal virus
Abstract:
Observations on the behavior of MHV (Pr) in the cerebral tissue of Princeton and Swiss weanling mice indicated a limited neurotropism. The virus migrated to the brain on intraperitoneal injection and was established there by cranial passage, though with difficulty in Swiss mice. Intracerebral multiplication was rarely followed by outward signs of nervous disorder. A slight pathologic reaction occurred in the brains of intracerebrally injected Princeton mice, but it was negligible compared with that of the ensuing hepatitis. In Swiss mice, injected intracerebrally with a mixture of MHV (Pr) and Eperythrozoon coccoides, a related virus with restricted pathogenicity and host range, possibly a mutant, was isolated from the liver and brain. MHV (C), an actively hepatotropic virus recovered from leukemic Balb C mice, was much more neurotropic than MHV (Pr). Intracerebral injection of Balb C and Swiss weanling mice was attended by marked leptomeningeal and encephalitic lesions. Paralysis of the extremities occurred in some of the animals. The virus was essentially inactive in Princeton mice. During the intracerebral passage of MHV (C) in Swiss mice a pleuropneumonia-like organism was isolated from the brain. In conjunction with the virus this organism produced a vigorous leukocytic reaction.
Insights
Murine hepatitis virus (MHV) strains show varied neurotropism. MHV (C) caused significant brain lesions and paralysis in mice, unlike MHV (Pr), highlighting differences in viral pathogenicity.
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- Murine hepatitis virus (MHV) is a significant pathogen in mice.
- Understanding MHV neurotropism is crucial for disease management and research.
- Different MHV strains exhibit varying host specificities and pathogenicity.
Purpose of the Study:
- To investigate the neurotropic potential of different MHV strains (MHV (Pr) and MHV (C)) in mice.
- To compare the neuropathological effects of MHV (Pr) and MHV (C) in various mouse strains.
- To identify potential co-factors influencing MHV neurotropism and pathogenicity.
Main Methods:
- Intraperitoneal and intracerebral injections of MHV (Pr) and MHV (C) into Princeton, Swiss, and Balb C weanling mice.
- Pathological examination of cerebral tissues to assess neurotropism and lesions.
- Isolation and identification of viral agents and co-infecting organisms (e.g., Eperythrozoon coccoides, pleuropneumonia-like organism).
Main Results:
- MHV (Pr) demonstrated limited neurotropism, establishing in the brain with difficulty and causing minimal pathology, overshadowed by hepatitis.
- MHV (C) exhibited significant neurotropism, inducing severe leptomeningeal and encephalitic lesions, paralysis, and high mortality in Balb C and Swiss mice, but was inactive in Princeton mice.
- Co-infection with Eperythrozoon coccoides or isolation of a pleuropneumonia-like organism during MHV (C) passage suggested potential modulation of host response.
Conclusions:
- MHV (C) is significantly more neurotropic and pathogenic than MHV (Pr), causing severe central nervous system disease in susceptible mouse strains.
- Mouse strain background (Princeton, Swiss, Balb C) critically influences susceptibility to MHV neurotropism and disease.
- The study underscores the diverse neuroinvasive capabilities within the MHV family and the potential role of co-infections in modulating disease presentation.
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