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Encephalomyocarditis virus can bind to and transfect non-permissive cells
Archives of Virology
|January 1, 1986
Summary
Rat cells block encephalomyocarditis virus (EMC virus) replication after attachment but before uncoating. This suggests the uncoating step is critical for EMC virus replication in permissive mouse cells.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Encephalomyocarditis virus (EMC virus) is an RNA virus with a broad host range.
- Cellular permissivity dictates viral replication efficiency.
- Understanding host-pathogen interactions is crucial for controlling viral infections.
Purpose of the Study:
- To investigate the cellular basis of differential permissivity to EMC virus infection between mouse and rat cells.
- To identify the specific stage of the viral replication cycle that is blocked in non-permissive rat cells.
Main Methods:
- Infection of permissive mouse embryo fibroblasts and mouse adrenal tumor cells with EMC virus.
- Infection of non-permissive rat glial and rat hepatoma cells with EMC virus.
- Assessment of viral attachment to both permissive and non-permissive cells.
- Transfection of rat cells with EMC virus RNA to assess replication post-attachment.
Main Results:
- Mouse cells supported EMC virus replication, while rat cells were non-permissive.
- EMC virus attached efficiently to both mouse and rat cells, ruling out attachment as the limiting factor.
- Transfection of rat cells with EMC virus RNA resulted in viral replication, indicating the block occurs post-attachment.
Conclusions:
- The non-permissivity of rat cells to EMC virus is not due to a failure of virus attachment.
- The replication block in rat cells occurs after virus entry but before or during the uncoating stage.
- These findings highlight the uncoating step as a potential determinant of EMC virus host range and replication.