Imperial College London

ProfessorPaiviOjala

Faculty of MedicineDepartment of Infectious Disease

Visiting Professor
 
 
 
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Contact

 

+44 (0)20 7594 3971p.ojala Website

 
 
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Location

 

443Medical SchoolSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Balistreri:2016:10.1371/journal.ppat.1005424,
author = {Balistreri, G and ViiliƤinen, J and Turunen, M and Diaz, R and Lyly, L and Pekkonen, P and Rantala, J and Ojala, K and Sarek, G and Teesalu, M and Denisova, O and Peltonen, K and Julkunen, I and Varjosalo, M and Kainov, D and Kallioniemi, O and Laiho, M and Taipale, J and Hautaniemi, S and Ojala, PM},
doi = {10.1371/journal.ppat.1005424},
journal = {Plos Pathogens},
title = {Oncogenic herpesvirus utilizes stress-induced cell cycle checkpoints for efficient lytic replication},
url = {http://dx.doi.org/10.1371/journal.ppat.1005424},
volume = {12},
year = {2016}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Kaposi's sarcoma herpesvirus (KSHV) causes Kaposi's sarcoma and certain lymphoproliferative malignancies. Latent infection is established in the majority of tumor cells, whereas lytic replication is reactivated in a small fraction of cells, which is important for both virus spread and disease progression. A siRNA screen for novel regulators of KSHV reactivation identified the E3 ubiquitin ligase MDM2 as a negative regulator of viral reactivation. Depletion of MDM2, a repressor of p53, favored efficient activation of the viral lytic transcription program and viral reactivation. During lytic replication cells activated a p53 response, accumulated DNA damage and arrested at G2-phase. Depletion of p21, a p53 target gene, restored cell cycle progression and thereby impaired the virus reactivation cascade delaying the onset of virus replication induced cytopathic effect. Herpesviruses are known to reactivate in response to different kinds of stress, and our study now highlights the molecular events in the stressed host cell that KSHV has evolved to utilize to ensure efficient viral lytic replication.
AU - Balistreri,G
AU - ViiliƤinen,J
AU - Turunen,M
AU - Diaz,R
AU - Lyly,L
AU - Pekkonen,P
AU - Rantala,J
AU - Ojala,K
AU - Sarek,G
AU - Teesalu,M
AU - Denisova,O
AU - Peltonen,K
AU - Julkunen,I
AU - Varjosalo,M
AU - Kainov,D
AU - Kallioniemi,O
AU - Laiho,M
AU - Taipale,J
AU - Hautaniemi,S
AU - Ojala,PM
DO - 10.1371/journal.ppat.1005424
PY - 2016///
SN - 1553-7374
TI - Oncogenic herpesvirus utilizes stress-induced cell cycle checkpoints for efficient lytic replication
T2 - Plos Pathogens
UR - http://dx.doi.org/10.1371/journal.ppat.1005424
UR - http://hdl.handle.net/10044/1/31189
VL - 12
ER -