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Rotavirus replication is correlated with S/G2 interphase arrest of the host cell cycle.

  • Glück S Institute of Virology, University of Zurich, Zurich, Switzerland.
  • Buttafuoco A Institute of Virology, University of Zurich, Zurich, Switzerland.
  • Meier AF Institute of Virology, University of Zurich, Zurich, Switzerland.
  • Arnoldi F Department of Medicine, Surgery and Health Sciences, University of Trieste, Trieste, Italy.
  • Vogt B Institute of Virology, University of Zurich, Zurich, Switzerland.
  • Schraner EM Institute of Virology, University of Zurich, Zurich, Switzerland.
  • Ackermann M Institute of Virology, University of Zurich, Zurich, Switzerland.
  • Eichwald C Institute of Virology, University of Zurich, Zurich, Switzerland.
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  • 2017-06-17
Published in:
  • PloS one. - 2017
Animals
Cyclin B1
Cytoskeleton
Dogs
G2 Phase Cell Cycle Checkpoints
HEK293 Cells
Humans
Kinesin
Macaca mulatta
Madin Darby Canine Kidney Cells
Rotavirus
S Phase Cell Cycle Checkpoints
Signal Transduction
Viral Proteins
Virus Replication
English In infected cells rotavirus (RV) replicates in viroplasms, cytosolic structures that require a stabilized microtubule (MT) network for their assembly, maintenance of the structure and perinuclear localization. Therefore, we hypothesized that RV could interfere with the MT-breakdown that takes place in mitosis during cell division. Using synchronized RV-permissive cells, we show that RV infection arrests the cell cycle in S/G2 phase, thus favoring replication by improving viroplasms formation, viral protein translation, and viral assembly. The arrest in S/G2 phase is independent of the host or viral strain and relies on active RV replication. RV infection causes cyclin B1 down-regulation, consistent with blocking entry into mitosis. With the aid of chemical inhibitors, the cytoskeleton network was linked to specific signaling pathways of the RV-induced cell cycle arrest. We found that upon RV infection Eg5 kinesin was delocalized from the pericentriolar region to the viroplasms. We used a MA104-Fucci system to identify three RV proteins (NSP3, NSP5, and VP2) involved in cell cycle arrest in the S-phase. Our data indicate that there is a strong correlation between the cell cycle arrest and RV replication.
Language
  • English
Open access status
gold
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Persistent URL
https://sonar.ch/global/documents/47607
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