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Imaging analysis of nuclear antiviral factors through direct detection of incoming adenovirus genome complexes.
Komatsu, Tetsuro; Will, Hans; Nagata, Kyosuke; Wodrich, Harald.
Affiliation
  • Komatsu T; Microbiologie Fondamentale et Pathogénicité, MFP CNRS UMR 5234, Université de Bordeaux, Bordeaux 33076, France; Department of Infection Biology, Faculty of Medicine, University of Tsukuba, Tsukuba 305-8575, Japan.
  • Will H; Department of Tumor Biology, University Hospital Hamburg-Eppendorf, 20246 Hamburg, Germany.
  • Nagata K; Department of Infection Biology, Faculty of Medicine, University of Tsukuba, Tsukuba 305-8575, Japan.
  • Wodrich H; Microbiologie Fondamentale et Pathogénicité, MFP CNRS UMR 5234, Université de Bordeaux, Bordeaux 33076, France. Electronic address: harald.wodrich@u-bordeaux.fr.
Biochem Biophys Res Commun ; 473(1): 200-205, 2016 Apr 22.
Article in En | MEDLINE | ID: mdl-27012198
ABSTRACT
Recent studies involving several viral systems have highlighted the importance of cellular intrinsic defense mechanisms through nuclear antiviral proteins that restrict viral propagation. These factors include among others components of PML nuclear bodies, the nuclear DNA sensor IFI16, and a potential restriction factor PHF13/SPOC1. For several nuclear replicating DNA viruses, it was shown that these factors sense and target viral genomes immediately upon nuclear import. In contrast to the anticipated view, we recently found that incoming adenoviral genomes are not targeted by PML nuclear bodies. Here we further explored cellular responses against adenoviral infection by focusing on specific conditions as well as additional nuclear antiviral factors. In line with our previous findings, we show that neither interferon treatment nor the use of specific isoforms of PML nuclear body components results in co-localization between incoming adenoviral genomes and the subnuclear domains. Furthermore, our imaging analyses indicated that neither IFI16 nor PHF13/SPOC1 are likely to target incoming adenoviral genomes. Thus our findings suggest that incoming adenoviral genomes may be able to escape from a large repertoire of nuclear antiviral mechanisms, providing a rationale for the efficient initiation of lytic replication cycle.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Phosphoproteins / Transcription Factors / Nuclear Proteins / Adenoviridae / Genome, Viral / DNA-Binding Proteins Type of study: Diagnostic_studies Limits: Humans Language: En Journal: Biochem Biophys Res Commun Year: 2016 Document type: Article Affiliation country: Japan

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Phosphoproteins / Transcription Factors / Nuclear Proteins / Adenoviridae / Genome, Viral / DNA-Binding Proteins Type of study: Diagnostic_studies Limits: Humans Language: En Journal: Biochem Biophys Res Commun Year: 2016 Document type: Article Affiliation country: Japan