Oncogenic Herpesvirus Utilizes Stress-Induced Cell Cycle Checkpoints for Efficient Lytic Replication
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 dise...
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| Veröffentlicht in: | PLOS PATHOGENS 2016-02, Vol.12 (2), p.e1005424-e1005424 |
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| creator | Balistreri, Giuseppe Viiliäinen, 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, Päivi M |
| description | 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. |
| doi_str_mv | 10.1371/journal.ppat.1005424 |
| format | Article |
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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.</description><identifier>ISSN: 1553-7374</identifier><identifier>ISSN: 1553-7366</identifier><identifier>EISSN: 1553-7374</identifier><identifier>DOI: 10.1371/journal.ppat.1005424</identifier><identifier>PMID: 26891221</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Biology and Life Sciences ; Cell cycle ; Cell Cycle Checkpoints - genetics ; Cell death ; Cell Line, Tumor ; DNA methylation ; DNA Replication ; Gene Expression Regulation, Viral - genetics ; Genetic aspects ; Health aspects ; Herpesvirus 8, Human - genetics ; Herpesviruses ; Humans ; Kaposis sarcoma ; Kinases ; Oncogenic viruses ; Research and Analysis Methods ; RNA, Small Interfering - genetics ; Sarcoma, Kaposi - metabolism ; Sarcoma, Kaposi - virology ; Stress, Physiological - genetics ; Tumor proteins ; Virus Activation - physiology ; Virus Latency - genetics ; Virus replication ; Virus Replication - genetics</subject><ispartof>PLOS PATHOGENS, 2016-02, Vol.12 (2), p.e1005424-e1005424</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Balistreri et al 2016 Balistreri et al</rights><rights>2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Balistreri G, Viiliäinen J, Turunen M, Diaz R, Lyly L, Pekkonen P, et al. (2016) Oncogenic Herpesvirus Utilizes Stress-Induced Cell Cycle Checkpoints for Efficient Lytic Replication. 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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. 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| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; SWEPUB Freely available online; PubMed Central Open Access |
| subjects | Biology and Life Sciences Cell cycle Cell Cycle Checkpoints - genetics Cell death Cell Line, Tumor DNA methylation DNA Replication Gene Expression Regulation, Viral - genetics Genetic aspects Health aspects Herpesvirus 8, Human - genetics Herpesviruses Humans Kaposis sarcoma Kinases Oncogenic viruses Research and Analysis Methods RNA, Small Interfering - genetics Sarcoma, Kaposi - metabolism Sarcoma, Kaposi - virology Stress, Physiological - genetics Tumor proteins Virus Activation - physiology Virus Latency - genetics Virus replication Virus Replication - genetics |
| title | Oncogenic Herpesvirus Utilizes Stress-Induced Cell Cycle Checkpoints for Efficient Lytic Replication |
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