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SV40 Utilizes ATM Kinase Activity to Prevent Non-homologous End Joining of Broken Viral DNA Replication Products
Viruses from both Polyomaviridae and Papillomaviridae families share several characteristics. These include common modes of DNA replication and an accumulation of DNA damage signaling and repair proteins at replicating viral DNA. Several DNA repair proteins, with unknown functions during viral DNA replication, associate with the viral replication centers of the polyomavirus simian virus 40 (SV40). In this study we examined the mechanisms that regulate and recruit DNA repair machinery to replicating viral DNA during permissive SV40 infection. We found that the virus deploys DNA repair to broken viral DNA using cellular DNA damage signaling pathways. Our results shed light on why both Polyomaviridae and Papillomaviridae DNA replication elicits DNA damage signaling and repair. As no effective treatments currently exist for the Polyomaviridae family, our data identify pathways that might be therapeutically targeted to inhibit productive viral replication. Additionally, we categorize distinct functions for DNA repair and damage signaling pathways during viral replication. The results provide insights into how viruses exploit cellular processes to overwhelm the cell and propagate.
Vyšlo v časopise: SV40 Utilizes ATM Kinase Activity to Prevent Non-homologous End Joining of Broken Viral DNA Replication Products. PLoS Pathog 10(12): e32767. doi:10.1371/journal.ppat.1004536
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004536Souhrn
Viruses from both Polyomaviridae and Papillomaviridae families share several characteristics. These include common modes of DNA replication and an accumulation of DNA damage signaling and repair proteins at replicating viral DNA. Several DNA repair proteins, with unknown functions during viral DNA replication, associate with the viral replication centers of the polyomavirus simian virus 40 (SV40). In this study we examined the mechanisms that regulate and recruit DNA repair machinery to replicating viral DNA during permissive SV40 infection. We found that the virus deploys DNA repair to broken viral DNA using cellular DNA damage signaling pathways. Our results shed light on why both Polyomaviridae and Papillomaviridae DNA replication elicits DNA damage signaling and repair. As no effective treatments currently exist for the Polyomaviridae family, our data identify pathways that might be therapeutically targeted to inhibit productive viral replication. Additionally, we categorize distinct functions for DNA repair and damage signaling pathways during viral replication. The results provide insights into how viruses exploit cellular processes to overwhelm the cell and propagate.
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Hygiena a epidemiológia Infekčné lekárstvo Laboratórium
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