Imaging analysis of nuclear antiviral factors through direct detection of incoming adenovirus genome complexes

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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.

in: BIOCHEM BIOPH RES CO, Jahrgang 473, Nr. 1, 22.04.2016, S. 200-5.

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@article{f51e114bf52645d9a4062075cd2defc0,
title = "Imaging analysis of nuclear antiviral factors through direct detection of incoming adenovirus genome complexes",
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.",
keywords = "Adenoviridae, Adenoviridae Infections, Cell Line, Tumor, DNA-Binding Proteins, Fluorescent Antibody Technique, Indirect, Genome, Viral, Host-Pathogen Interactions, Humans, Interferons, Microscopy, Fluorescence, Neutrophils, Nuclear Proteins, Phosphoproteins, Transcription Factors, Virus Replication, Journal Article, Research Support, Non-U.S. Gov't",
author = "Tetsuro Komatsu and Hans Will and Kyosuke Nagata and Harald Wodrich",
note = "Copyright {\textcopyright} 2016 Elsevier Inc. All rights reserved.",
year = "2016",
month = apr,
day = "22",
doi = "10.1016/j.bbrc.2016.03.078",
language = "English",
volume = "473",
pages = "200--5",
journal = "BIOCHEM BIOPH RES CO",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Imaging analysis of nuclear antiviral factors through direct detection of incoming adenovirus genome complexes

AU - Komatsu, Tetsuro

AU - Will, Hans

AU - Nagata, Kyosuke

AU - Wodrich, Harald

N1 - Copyright © 2016 Elsevier Inc. All rights reserved.

PY - 2016/4/22

Y1 - 2016/4/22

N2 - 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.

AB - 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.

KW - Adenoviridae

KW - Adenoviridae Infections

KW - Cell Line, Tumor

KW - DNA-Binding Proteins

KW - Fluorescent Antibody Technique, Indirect

KW - Genome, Viral

KW - Host-Pathogen Interactions

KW - Humans

KW - Interferons

KW - Microscopy, Fluorescence

KW - Neutrophils

KW - Nuclear Proteins

KW - Phosphoproteins

KW - Transcription Factors

KW - Virus Replication

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.bbrc.2016.03.078

DO - 10.1016/j.bbrc.2016.03.078

M3 - SCORING: Journal article

C2 - 27012198

VL - 473

SP - 200

EP - 205

JO - BIOCHEM BIOPH RES CO

JF - BIOCHEM BIOPH RES CO

SN - 0006-291X

IS - 1

ER -