Oncogenic Herpesvirus Utilizes Stress-Induced Cell Cycle Checkpoints for Efficient Lytic Replication

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Balistreri , G , Viiliainen , J , Turunen , M , Diaz , R , Lyly , L , Pekkonen , P , Rantala , J , Ojala , K , Sarek , G , Teesalu , M , Denisova , O , Peltonen , K , Julkunen , I , Varjosalo , M , Kainov , D , Kallioniemi , O , Laiho , M , Taipale , J , Hautaniemi , S & Ojala , P M 2016 , ' Oncogenic Herpesvirus Utilizes Stress-Induced Cell Cycle Checkpoints for Efficient Lytic Replication ' , PLoS Pathogens , vol. 12 , no. 2 , 1005424 . https://doi.org/10.1371/journal.ppat.1005424

Title: Oncogenic Herpesvirus Utilizes Stress-Induced Cell Cycle Checkpoints for Efficient Lytic Replication
Author: Balistreri, Giuseppe; Viiliainen, Johanna; Turunen, Mikko; Diaz, Raquel; Lyly, Lauri; Pekkonen, Pirita; Rantala, Juha; Ojala, Krista; Sarek, Grzegorz; Teesalu, Mari; Denisova, Oxana; Peltonen, Karita; Julkunen, Ilkka; Varjosalo, Markku; Kainov, Denis; Kallioniemi, Olli; Laiho, Marikki; Taipale, Jussi; Hautaniemi, Sampsa; Ojala, Paivi M.
Contributor organization: Research Programs Unit
Translational Cancer Biology (TCB) Research Programme
Genome-Scale Biology (GSB) Research Program
Department of Pathology
Medicum
Nutrient sensing laboratory
Institute for Molecular Medicine Finland
Faculty of Pharmacy
Molecular Systems Biology
Denis Kainov / Principal Investigator
Olli-Pekka Kallioniemi / Principal Investigator
Jussi Taipale / Principal Investigator
Sampsa Hautaniemi / Principal Investigator
Bioinformatics
Drug Research Program
ImmunoViroTherapy Lab
Date: 2016-02
Language: eng
Number of pages: 26
Belongs to series: PLoS Pathogens
ISSN: 1553-7366
DOI: https://doi.org/10.1371/journal.ppat.1005424
URI: http://hdl.handle.net/10138/165104
Abstract: 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.
Subject: SARCOMA-ASSOCIATED HERPESVIRUS
EPSTEIN-BARR-VIRUS
MITOTIC CHROMOSOME CONDENSATION
HISTONE H3 PHOSPHORYLATION
DNA-DAMAGE CHECKPOINT
BREAST-CANCER CELLS
KAPOSIS-SARCOMA
GENE-EXPRESSION
NUCLEAR ANTIGEN
INDUCED LYMPHOMAS
3111 Biomedicine
Peer reviewed: Yes
Rights: cc_by
Usage restriction: openAccess
Self-archived version: publishedVersion


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