Herpes simplex virus 1 induces egress channels through marginalized host chromatin
Myllys, M., Ruokolainen, V., Aho, V., Smith, E. A., Hakanen, S., Peri, P., Salvetti, A., Timonen, J., Hukkanen, V., Larabell, C. A., & Vihinen-Ranta, M. (2016). Herpes simplex virus 1 induces egress channels through marginalized host chromatin. Scientific Reports, 6, Article 28844. https://doi.org/10.1038/srep28844
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Scientific ReportsAuthors
Date
2016Discipline
Solu- ja molekyylibiologiaFysiikkaNanoscience CenterCell and Molecular BiologyPhysicsNanoscience CenterCopyright
© the Authors, 2016. This is an open access article published by Nature. This work is licensed under a Creative Commons Attribution 4.0 International License.
Lytic infection with herpes simplex virus type 1 (HSV-1) induces profound modification of the cell
nucleus including formation of a viral replication compartment and chromatin marginalization into
the nuclear periphery. We used three-dimensional soft X-ray tomography, combined with cryogenic
fluorescence, confocal and electron microscopy, to analyse the transformation of peripheral chromatin
during HSV-1 infection. Our data showed an increased presence of low-density gaps in the marginalized
chromatin at late infection. Advanced data analysis indicated the formation of virus-nucleocapsid-sized
(or wider) channels extending through the compacted chromatin of the host. Importantly, confocal
and electron microscopy analysis showed that these gaps frequently contained viral nucleocapsids.
These results demonstrated that HSV-1 infection induces the formation of channels penetrating the
compacted layer of cellular chromatin and allowing for the passage of progeny viruses to the nuclear
envelope, their site of nuclear egress.
...
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Nature Publishing GroupISSN Search the Publication Forum
2045-2322Keywords
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