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Berlin Brandenburg

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  • 1
    Language: English
    In: Reviews in medical virology, May 2011, Vol.21(3), pp.154-80
    Description: Herpesvirus infections of humans can cause a broad variety of symptoms ranging from mild afflictions to life-threatening disease. During infection, the large double-stranded DNA genomes of all herpesviruses are transcribed, replicated and encapsidated in the host cell nucleus, where DNA is typically structured and manoeuvred through nucleosomes. Nucleosomes individually assemble DNA around core histone octamers to form 'beads-on-a-string' chromatin fibres. Herpesviruses have responded to the advantages and challenges of chromatin formation in biologically unique ways. Although herpesvirus DNA is devoid of histones within nucleocapsids, nuclear viral genomes most likely form irregularly arranged or unstable nucleosomes during productive infection, and regular nucleosomal arrays resembling host cell chromatin in latently infected cells. Besides variations in nucleosome density, herpesvirus chromatin 'bead strings' undergo dynamic changes in histone composition and modification during the different stages of productive replication, latent infection and reactivation from latency, raising the likely possibility that epigenetic processes may dictate, at least in part, the outcome of infection and ensuing pathogenesis. Here, we summarise and discuss several new and important aspects regarding the nucleosome-based mechanisms that regulate herpesvirus chromatin structure and function in infected cells. Special emphasis is given to processes of histone deposition, histone variant exchange and covalent histone modification in relation to the transcription from the viral genome during productive and latent infections by human cytomegalovirus and herpes simplex virus type 1. We also present an overview on emerging histone-directed antiviral strategies that may be developed into 'epigenetic therapies' to improve current prevention and treatment options targeting herpesvirus infection and disease.
    Keywords: Virus Replication ; Chromatin -- Metabolism ; Cytomegalovirus -- Physiology ; DNA, Viral -- Metabolism ; Herpesvirus 1, Human -- Physiology ; Histones -- Metabolism ; Nucleosomes -- Metabolism
    E-ISSN: 1099-1654
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  • 2
    Language: English
    In: Reviews in Medical Virology, January 2010, Vol.20(1), pp.34-50
    Description: The double‐stranded DNA genomes of herpesviruses exist in at least three alternative global chromatin states characterised by distinct nucleosome content. When encapsidated in virus particles, the viral DNA is devoid of any nucleosomes. In contrast, within latently infected nuclei herpesvirus genomes are believed to form regular nucleosomal structures resembling cellular chromatin. Finally, during productive infection nuclear viral DNA appears to adopt a state of intermediate chromatin formation with irregularly spaced nucleosomes. Nucleosome occupancy coupled with posttranslational histone modifications and other epigenetic marks may contribute significantly to the extent and timing of transcription from the viral genome and, consequently, to the outcome of infection. Recent research has provided first insights into the viral and cellular mechanisms that either maintain individual herpesvirus chromatin states or mediate transition between them. Here, we summarise and discuss both early work and new developments pointing towards common principles pertinent to the dynamic structure and epigenetic regulation of herpesvirus chromatin. Special emphasis is given to the emerging similarities in nucleosome assembly and disassembly processes on herpes simplex virus type 1 and human cytomegalovirus genomes over the course of the viral productive replication cycle and during the switch between latent and lytic infectious stages. Copyright © 2009 John Wiley & Sons, Ltd.
    Keywords: Genomes ; Latent Infection ; Nucleosomes ; Histones ; Chromatin ; Replication ; Epigenetics ; DNA ; Transcription ; Nuclei ; Infection ; Human Cytomegalovirus ; Herpesvirus ; Herpes Simplex Virus 1 ; Human Cytomegalovirus ; Herpesvirus ; Herpes Simplex Virus 1 ; Chromatin ; DNA ; Genomes ; Histones ; Infection ; Latent Infection ; Nuclei ; Nucleosomes ; Replication ; Transcription ; Epigenetics ; Replication;
    ISSN: 1052-9276
    E-ISSN: 1099-1654
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