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@ARTICLE{Lewis:601642,
      author       = {Lewis, Hannah C. and Kelnhofer-Millevolte, Laurel E. and
                      Brinkley, Mia R. and Arbach, Hannah E. and Arnold, Edward A.
                      and Sanders, Saskia and Bosse, Jens Bernhard and
                      Ramachandran, Srinivas and Avgousti, Daphne C.},
      title        = {{HSV}-1 exploits host heterochromatin for nuclear egress},
      journal      = {The journal of cell biology},
      volume       = {222},
      number       = {9},
      issn         = {0021-9525},
      address      = {New York, NY},
      publisher    = {Rockefeller Univ. Press},
      reportid     = {PUBDB-2024-00335},
      pages        = {e202304106},
      year         = {2023},
      abstract     = {Herpes simplex virus (HSV-1) progeny form in the nucleus
                      and exit to successfully infect other cells. Newly formed
                      capsids navigate complex chromatin architecture to reach the
                      inner nuclear membrane (INM) and egress. Here, we
                      demonstrate by transmission electron microscopy (TEM) that
                      HSV-1 capsids traverse heterochromatin associated with
                      trimethylation on histone H3 lysine 27 (H3K27me3) and the
                      histone variant macroH2A1. Through chromatin profiling
                      during infection, we revealed global redistribution of these
                      marks whereby massive host genomic regions bound by
                      macroH2A1 and H3K27me3 correlate with decreased host
                      transcription in active compartments. We found that the loss
                      of these markers resulted in significantly lower viral
                      titers but did not impact viral genome or protein
                      accumulation. Strikingly, we discovered that loss of
                      macroH2A1 or H3K27me3 resulted in nuclear trapping of
                      capsids. Finally, by live-capsid tracking, we quantified
                      this decreased capsid movement. Thus, our work demonstrates
                      that HSV-1 takes advantage of the dynamic nature of host
                      heterochromatin formation during infection for efficient
                      nuclear egress.},
      cin          = {CSSB-MHH-JB},
      ddc          = {570},
      cid          = {I:(DE-H253)CSSB-MHH-JB-20210520},
      pnm          = {899 - ohne Topic (POF4-899) / DFG project 390874280 - EXC
                      2155: RESIST - Resolving Infection Susceptibility
                      (390874280) / DFG project 443644894 - FOR 5200: Disrupt -
                      Evade - Exploit: Steuerung der Genexpression und
                      Wirtsantwort durch DNA Viren (DEEP-DV) (443644894)},
      pid          = {G:(DE-HGF)POF4-899 / G:(GEPRIS)390874280 /
                      G:(GEPRIS)443644894},
      experiment   = {EXP:(DE-MLZ)NOSPEC-20140101},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37516914},
      UT           = {WOS:001068239900001},
      doi          = {10.1083/jcb.202304106},
      url          = {https://bib-pubdb1.desy.de/record/601642},
}