Borna Disease Virus Nucleoprotein Interacts with the Cdc2-Cyclin B1 Complex
AUTOR(ES)
Planz, Oliver
FONTE
American Society for Microbiology
RESUMO
Transition from G2 to M phase, a cell cycle checkpoint, is regulated by the Cdc2-cyclin B1 complex. Here, we report that persistent infection with Borna disease virus (BDV), a noncytolytic RNA virus infecting the central nervous system, results in decelerated proliferation of infected host cells due to a delayed G2-to-M transition. Persistent BDV-infected rat fibroblast cells showed reduced proliferation compared to uninfected cells. In pull-down assays we observed an interaction of the viral nucleoprotein with the Cdc2-cyclin B1 complex. Transfection of the viral nucleoprotein but not of the phosphoprotein also results in decelerated proliferation. This phenomenon was found in BDV-susceptible primary rat fibroblast cells and also in primary mouse cells, which are not susceptible to BDV infection. This is the first evidence that the noncytolytic Borna disease virus can manipulate host cell functions via interaction of the viral nucleoprotein with mitotic entry regulators. BDV preferentially infects and persists in nondividing neurons. The present report could give an explanation for this selective choice of host cell by BDV.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=224960Documentos Relacionados
- Overproduction of Human Myt1 Kinase Induces a G2 Cell Cycle Delay by Interfering with the Intracellular Trafficking of Cdc2-Cyclin B1 Complexes
- Cdc2–cyclin B kinase activity links Crb2 and Rqh1–topoisomerase III
- Initial activation of cyclin-B1–cdc2 kinase requires phosphorylation of cyclin B1
- Localization and Dynamics of Cdc2-Cyclin B during Meiotic Reinitiation in Starfish OocytesV⃞
- Linker Histones Stimulate HSPA2 ATPase Activity Through NASP Binding and Inhibit CDC2/Cyclin B1 Complex Formation During Meiosis in the Mouse1