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Updated: Mar 23, 2026
Isolation of Viral Replication Compartment-enriched Sub-nuclear Fractions from Adenovirus-infected Normal Human Cells
Published on: November 12, 2015
Imaging analysis of nuclear antiviral factors through direct detection of incoming adenovirus genome complexes
Tetsuro Komatsu1, Hans Will2, Kyosuke Nagata3
1Microbiologie 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.
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.
Insights
Incoming adenoviral genomes evade nuclear antiviral defenses, including PML nuclear bodies, IFI16, and PHF13/SPOC1. This evasion explains the efficient initiation of adenovirus lytic replication.
Area of Science:
- Virology
- Cellular Biology
- Immunology
Background:
- Cellular intrinsic defense mechanisms utilize nuclear antiviral proteins to restrict viral propagation.
- Factors like PML nuclear bodies, IFI16, and PHF13/SPOC1 target viral genomes upon nuclear import for DNA viruses.
- Adenoviral genomes were previously found not to be targeted by PML nuclear bodies upon entry.
Purpose of the Study:
- To further investigate cellular responses against adenoviral infection.
- To explore additional nuclear antiviral factors and specific conditions affecting adenoviral entry.
- To determine if incoming adenoviral genomes are targeted by known nuclear antiviral proteins.
Main Methods:
- Confocal microscopy to analyze co-localization of adenoviral genomes with subnuclear domains.
- Imaging analyses to assess the interaction of adenoviral genomes with IFI16 and PHF13/SPOC1.
- Infection of cells under specific conditions, including interferon treatment.
Main Results:
- Incoming adenoviral genomes did not co-localize with PML nuclear body components, even with interferon treatment or specific PML isoforms.
- Neither IFI16 nor PHF13/SPOC1 were found to target incoming adenoviral genomes.
- Adenoviral genomes appear to escape established nuclear antiviral surveillance mechanisms.
Conclusions:
- Incoming adenoviral genomes evade a significant repertoire of nuclear antiviral mechanisms.
- This evasion provides a mechanistic explanation for the efficient initiation of the adenoviral lytic replication cycle.
- Further research is needed to identify the specific mechanisms by which adenoviruses evade nuclear defenses.
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