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Host age and cell type influence measles virus protein expression in the central nervous system
1Department of Neurology, University of Maryland School of Medicine, Baltimore 21201.
Abstract:
Measles virus infection of the central nervous system (CNS) of children can result in a slow, progressive fatal disease, subacute sclerosing panencephalitis (SSPE). The pathogenesis of persistent measles virus infection of the CNS has been studied by comparing viral protein expression in suckling or weanling hamsters infected with the HBS strain of measles virus. Suckling animals develop a rapidly progressive fatal encephalitis while weanling animals survive and are persistently infected. Viral nucleocapsid (NP) and hemagglutinin (H) proteins have been examined during acute infection in suckling and weanling animals. Viral H protein expression is selectively inhibited in infected neurons of weanling animals, while infected ependymal cells retain the capability to express H protein at the cell surface; suckling animals express high levels of both proteins. Anti-measles antibodies are not responsible for the inhibition of H protein since immunosuppression does not restore protein expression. The cell-associated virus which is recovered late in infection by co-cultivation with Vero cells expresses all viral proteins. These results suggest that intact viral genome is present in persistent infections, and cell type or state of differentiation of infected cells may be instrumental in expression of viral proteins which can influence lytic or persistent outcome of infection.
Insights
Measles virus infection can cause subacute sclerosing panencephalitis (SSPE). Viral hemagglutinin protein expression is inhibited in neurons of persistently infected weanling hamsters, influencing disease outcome.
Area of Science:
- Neurovirology
- Infectious Diseases
- Molecular Virology
Background:
- Measles virus can cause persistent central nervous system (CNS) infections, leading to subacute sclerosing panencephalitis (SSPE), a fatal neurological disease.
- Understanding the mechanisms of persistent measles virus CNS infection is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the pathogenesis of persistent measles virus infection in the CNS.
- To compare viral protein expression in suckling and weanling hamsters infected with measles virus.
Main Methods:
- Infection of suckling and weanling hamsters with the HBS strain of measles virus.
- Analysis of viral nucleocapsid (NP) and hemagglutinin (H) protein expression in infected CNS tissues.
- Assessment of viral protein expression in neurons and ependymal cells.
- Evaluation of the role of anti-measles antibodies and cell type in viral protein expression.
Main Results:
- Suckling hamsters developed rapidly fatal encephalitis, while weanling hamsters showed persistent infection.
- Viral hemagglutinin (H) protein expression was selectively inhibited in infected neurons of weanling hamsters, but not in ependymal cells.
- Immunosuppression did not restore H protein expression, indicating antibodies were not responsible for inhibition.
- Cell-associated virus recovered late in infection expressed all viral proteins.
Conclusions:
- Persistent measles virus CNS infections involve an intact viral genome.
- Cell type and differentiation state of infected cells play a critical role in regulating viral protein expression.
- Differential viral protein expression influences the outcome of measles virus infection, determining lytic or persistent disease.