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Published on: December 9, 2014
Tioman virus infection in experimentally infected mouse brain and its association with apoptosis
Koon Chu Yaiw1, Kien Chai Ong, Kaw Bing Chua
1Department of Pathology, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia.
Abstract:
Tioman virus is a newly described bat-urine derived paramyxovirus isolated in Tioman Island, Malaysia in 2001. Hitherto, neither human nor animal infection by this virus has been reported. Nonetheless, its close relationship to another paramyxovirus, the Menangle virus which had caused diseases in humans and pigs [Philbey, A.W., Kirkland, P.D., Ross, A.D., Davis, R.J., Gleeson, A.B., Love, R.J., Daniels, P.W., Gould, A.R., Hyatt, A.D., 1998. An apparently new virus (family Paramyxoviridae) infectious for pigs, humans, and fruit bats. Emerg. Infect. Dis. 4, 269-271], raises the possibility that it may be potentially pathogenic. In this study, mice were experimentally infected with Tioman virus by intraperitoneal and intracerebral routes, and the cellular targets and topographical distribution of viral genome and antigens were examined using in situ hybridization and immunohistochemistry, respectively. The possible association between viral infection and apoptosis was also investigated using the TUNEL assay and immunohistochemistry to FasL, Caspase-3, Caspase-8, Caspase-9 and bcl-2. The results showed that Tioman virus inoculated intracerebrally was neurotropic causing plaque-like necrotic areas, and appeared to preferentially replicate in the neocortex and limbic system. Viral infection of inflammatory cells was also demonstrated. TUNEL and Caspase-3 positivity was found in inflammatory cells but not in neurons, while FasL, Caspase-8 and Caspase-9 were consistently negative. This suggests that neuronal infection was associated with necrosis rather than apoptosis. Moreover, the data suggest that there may be an association between viral infection and apoptosis in inflammatory cells, and that it could, at least in part, involve Caspase-independent pathways. Bcl-2 was expressed in some neurons and inflammatory cells indicating its possible role in anti-apoptosis. There was no evidence of central nervous system infection via the intraperitoneal route.
Insights
Tioman virus, a bat-derived paramyxovirus, was found to be neurotropic in mice, infecting the brain's neocortex and limbic system. Neuronal infection led to necrosis, while inflammatory cells showed apoptosis, suggesting complex viral interactions.
Area of Science:
- Virology
- Pathology
- Neuroscience
Background:
- Tioman virus is a newly identified paramyxovirus from bat urine.
- Its close relation to the pathogenic Menangle virus suggests potential risks.
- No human or animal infections have been previously reported.
Purpose of the Study:
- To investigate the pathogenicity and neurotropic potential of Tioman virus in a mouse model.
- To determine the cellular targets and distribution of Tioman virus in infected mice.
- To explore the association between Tioman virus infection and apoptosis.
Main Methods:
- Mice were infected with Tioman virus via intraperitoneal and intracerebral routes.
- In situ hybridization and immunohistochemistry were used to detect viral genome and antigens.
- TUNEL assay and immunohistochemistry for apoptosis markers (FasL, Caspase-3, -8, -9, bcl-2) were performed.
Main Results:
- Intracerebral inoculation resulted in neurotropism, with Tioman virus replicating in the neocortex and limbic system, causing necrotic lesions.
- Viral infection was observed in inflammatory cells, which exhibited positivity for TUNEL and Caspase-3, suggesting apoptosis.
- Neuronal infection was linked to necrosis, not apoptosis, and Caspase-independent pathways may be involved in inflammatory cell apoptosis. Bcl-2 expression indicated an anti-apoptotic role.
Conclusions:
- Tioman virus is neurotropic, primarily affecting the neocortex and limbic system following intracerebral infection.
- Neuronal damage appears to be necrosis-driven, while inflammatory cells undergo apoptosis through potentially Caspase-independent mechanisms.
- The intraperitoneal route did not lead to central nervous system infection in this study.
