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Title: Herpes simplex virus 1 induces egress channels through marginalized host chromatin

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. Here, 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. Our 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.
Authors:
 [1] ;  [2] ;  [1] ;  [3] ;  [2] ;  [4] ;  [5] ;  [6] ;  [4] ;  [7] ;  [2]
  1. Univ. of Jyvaskyla (Finland). Dept. of Physics and Nanoscience Center
  2. Univ. of Jyvaskyla (Finland). Dept. of Biological and Environmental Science and Nanoscience Center
  3. Univ. of California, San Francisco, CA (United States). Dept. of Anatomy; Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States)
  4. Univ. of Turku (Finland)
  5. International Center for Research in Infectiology, Lyon (France); Ecole Normale Superieure, Lyon (France); Univ. of Lyon (France). LabEx Ecofect
  6. Univ. of Jyvaskyla (Finland). Dept. of Physics and Nanoscience Center; ITMO uUniv., St. Petersburg (Russia)
  7. Univ. of California, San Francisco, CA (United States). Dept. of Anatomy; Univ. of Turku (Finland)
Publication Date:
Grant/Contract Number:
AC02-05CH11231
Type:
Accepted Manuscript
Journal Name:
Scientific Reports
Additional Journal Information:
Journal Volume: 6; Journal Issue: 1; Journal ID: ISSN 2045-2322
Publisher:
Nature Publishing Group
Research Org:
Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States)
Sponsoring Org:
USDOE Office of Science (SC), Biological and Environmental Research (BER) (SC-23)
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; 60 APPLIED LIFE SCIENCES; herpes virus; nuclear organization
OSTI Identifier:
1414761

Myllys, Markko, Ruokolainen, Visa, Aho, Vesa, Smith, Elizabeth A., Hakanen, Satu, Peri, Piritta, Salvetti, Anna, Timonen, Jussi, Hukkanen, Veijo, Larabell, Carolyn A., and Vihinen-Ranta, Maija. Herpes simplex virus 1 induces egress channels through marginalized host chromatin. United States: N. p., Web. doi:10.1038/srep28844.
Myllys, Markko, Ruokolainen, Visa, Aho, Vesa, Smith, Elizabeth A., Hakanen, Satu, Peri, Piritta, Salvetti, Anna, Timonen, Jussi, Hukkanen, Veijo, Larabell, Carolyn A., & Vihinen-Ranta, Maija. Herpes simplex virus 1 induces egress channels through marginalized host chromatin. United States. doi:10.1038/srep28844.
Myllys, Markko, Ruokolainen, Visa, Aho, Vesa, Smith, Elizabeth A., Hakanen, Satu, Peri, Piritta, Salvetti, Anna, Timonen, Jussi, Hukkanen, Veijo, Larabell, Carolyn A., and Vihinen-Ranta, Maija. 2016. "Herpes simplex virus 1 induces egress channels through marginalized host chromatin". United States. doi:10.1038/srep28844. https://www.osti.gov/servlets/purl/1414761.
@article{osti_1414761,
title = {Herpes simplex virus 1 induces egress channels through marginalized host chromatin},
author = {Myllys, Markko and Ruokolainen, Visa and Aho, Vesa and Smith, Elizabeth A. and Hakanen, Satu and Peri, Piritta and Salvetti, Anna and Timonen, Jussi and Hukkanen, Veijo and Larabell, Carolyn A. and Vihinen-Ranta, Maija},
abstractNote = {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. Here, 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. Our 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.},
doi = {10.1038/srep28844},
journal = {Scientific Reports},
number = 1,
volume = 6,
place = {United States},
year = {2016},
month = {6}
}