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Published on: November 18, 2010
Invasion of mouse brain by Mount Elgon bat virus
Abstract:
Mount Elgon bat virus killed mice up to 13 days of age when given intranasally. Virus reached the brain of these mice via the olfactory nerve route without obvious multiplication in any tissues other than the nasal mucosa of 1- to 6-day-old mice and in the absence of viraemia or circulating virus neutralizing antibody. Large amounts of interferon were, however, synthesized in brain where virus grew to high titres. In mice older than 13 days virus did not multiply in brain but it reached the olfactory bulbs and persisted until virus neutralizing antibody appeared in the nasopharynx. No antibody was detected in blood of the resistant mice, nor was interferon detected in their brains or nasal mucosa. Immunosuppression of the resistant mice with cyclophosphamide resulted in moderate virus growth in mid- and hind-brain accompanied by interferon synthesis and death of the mice. The local immune response prevented invasion of mid- and hind-brain in the resistant mice.
Insights
Mount Elgon bat virus is lethal to young mice via the olfactory nerve route. Older mice resist infection due to a local immune response, preventing brain invasion.
Area of Science:
- Virology
- Immunology
- Neuroscience
Background:
- Mount Elgon bat virus (MEBV) is a bat-borne virus with potential zoonotic implications.
- Understanding the pathogenesis and host-virus interactions is crucial for assessing public health risks.
Purpose of the Study:
- To investigate the age-dependent susceptibility of mice to MEBV infection.
- To elucidate the viral route of entry, replication sites, and the role of the immune response in determining disease outcome.
Main Methods:
- Intranasal inoculation of MEBV in mice of varying ages (1-day to adult).
- Analysis of viral distribution in tissues (brain, nasal mucosa) via olfactory nerve.
- Assessment of immune markers: interferon synthesis and virus-neutralizing antibody production.
- Evaluation of immunosuppression effects using cyclophosphamide.
Main Results:
- MEBV caused mortality in mice up to 13 days old, primarily through olfactory nerve entry to the brain.
- In young mice, virus replicated in nasal mucosa and brain, with high interferon levels.
- Older mice showed resistance; virus reached olfactory bulbs but did not multiply in the brain.
- Resistant mice lacked detectable blood antibodies and brain/nasal interferon; immunosuppression led to severe disease.
Conclusions:
- Age-related resistance to MEBV is mediated by a local immune response preventing central nervous system invasion.
- Interferon synthesis in the brain is associated with viral replication and susceptibility.
- The olfactory nerve serves as a critical route for MEBV neuroinvasion.
