Intracellular dynamics of actin affects Borna disease virus replication in the nucleus
•Inhibition of the nucleocytoplasmic transport of actin affects BoDV replication.•Nuclear accumulation of actin results in the structural aberration in intranuclear viral factories of BoDV.•Inhibition of nuclear export of actin promotes the accumulation of viral proteins in the cytoplasm. Borna dise...
Gespeichert in:
Veröffentlicht in: | Virus research 2019-04, Vol.263, p.179-183 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | •Inhibition of the nucleocytoplasmic transport of actin affects BoDV replication.•Nuclear accumulation of actin results in the structural aberration in intranuclear viral factories of BoDV.•Inhibition of nuclear export of actin promotes the accumulation of viral proteins in the cytoplasm.
Borna disease virus (BoDV) is a nonsegmented, negative-strand RNA virus that uniquely replicates and establishes persistent infection in cell nucleus. Recent studies have demonstrated the presence of actin in the nucleus and its role in intranuclear phenomena such as transcription and DNA repair. Although nuclear actin is involved in the life cycle of some intranuclear DNA viruses, the interaction between BoDV and nuclear actin has not been reported. In this study, we show that the inhibition of the nucleocytoplasmic transport of actin affects the replication of BoDV in the nucleus. The knockdown of a nuclear export factor of actin, exportin 6, results in the induction of structural aberration in intranuclear viral factories of BoDV. Furthermore, the inhibition of the nuclear export of actin promotes accumulation of viral matrix protein in the cytoplasm and periphery of the infected cells. These results suggest that the dynamics of actin affect the replication of BoDV by disturbing the structure of viral factories in the nucleus. |
---|---|
ISSN: | 0168-1702 1872-7492 |
DOI: | 10.1016/j.virusres.2019.02.004 |