Open AccessBorna Disease Virus Nucleoprotein Interacts with the Cdc2-Cyclin B1 Complex
Author(s) -
Oliver Planz,
Stephan Pleschka,
Katja Oesterle,
Friederike BerberichSiebelt,
Christina Ehrhardt,
Lothar Stitz,
Stephan Ludwig
Publication year - 2003
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.77.20.11186-11192.2003
Subject(s) - biology , nucleoprotein , virology , phosphoprotein , cyclin b1 , virus , cyclin dependent kinase 1 , microbiology and biotechnology , cell cycle , cell , phosphorylation , genetics
Transition from G(2) 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 G(2)-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.