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Sci Rep. 2016 Jun 28;6:28844. doi: 10.1038/srep28844.

Herpes simplex virus 1 induces egress channels through marginalized host chromatin.

Author information

1
University of Jyvaskyla, Department of Physics and Nanoscience Center, Jyvaskyla, FI-40500, Finland.
2
University of Jyvaskyla, Department of Biological and Environmental Science and Nanoscience Center, Jyvaskyla, FI-40500, Finland.
3
Department of Anatomy, University of California San Francisco, San Francisco, CA, 94158, USA.
4
Physical Biosciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA, 94720, USA.
5
University of Turku, Turku, Finland.
6
International Center for Research in Infectiology (CIRI), INSERM U1111, CNRS UMR5308, Lyon, F-69007, France.
7
Ecole Normale Supérieure de Lyon, Lyon F-69007, France.
8
Université de Lyon, UCB-Lyon1, Lyon, F-69007, France.
9
LabEx Ecofect, Université de Lyon, Lyon, F-69007, France.
10
ITMO University, Kronverkskii ave. 49, 197101, Saint Petersburg, Russia.

Abstract

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.

PMID:
27349677
PMCID:
PMC5378911
DOI:
10.1038/srep28844
[Indexed for MEDLINE]
Free PMC Article

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