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Borna disease virus nucleoprotein interacts with the CDC2-cyclin B1 complex
Oliver Planz1, Stephan Pleschka, Katja Oesterle
1Institut für Immunologie, Bundesforschungsanstalt für Viruskrankheiten der Tiere, Tübingen, Germany. oliver.planz@tue.bfav.de
Journal of Virology
|September 27, 2003
Summary
Borna disease virus (BDV) infection slows host cell proliferation by delaying the G(2)-to-M cell cycle transition. The viral nucleoprotein interacts with Cdc2-cyclin B1, impacting cell division.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- The transition from G(2) to M phase is a critical checkpoint in the cell cycle, regulated by the Cdc2-cyclin B1 complex.
- Borna disease virus (BDV) is a noncytolytic RNA virus that infects the central nervous system.
Purpose of the Study:
- To investigate the effect of persistent Borna disease virus infection on host cell proliferation.
- To identify the viral components and mechanisms involved in modulating cell cycle progression.
Main Methods:
- Comparative proliferation assays of BDV-infected and uninfected rat fibroblast cells.
- Pull-down assays to detect interactions between viral proteins and the Cdc2-cyclin B1 complex.
- Transfection experiments using viral nucleoprotein and phosphoprotein.
Main Results:
- Persistent BDV infection decelerated host cell proliferation due to a delayed G(2)-to-M transition.
- An interaction was observed between the viral nucleoprotein and the Cdc2-cyclin B1 complex.
- Transfection with viral nucleoprotein, but not phosphoprotein, also resulted in decelerated proliferation.
Conclusions:
- Borna disease virus manipulates host cell functions by interacting with mitotic entry regulators via its nucleoprotein.
- This interaction provides a potential explanation for BDV's preferential infection of non-dividing neurons.