Literature DB >> 18264117

Chromatin control of herpes simplex virus lytic and latent infection.

David M Knipe1, Anna Cliffe.   

Abstract

Herpes simplex viruses (HSV) can undergo a lytic infection in epithelial cells and a latent infection in sensory neurons. During latency the virus persists until reactivation, which leads to recurrent productive infection and transmission to a new host. How does HSV undergo such different types of infection in different cell types? Recent research indicates that regulation of the assembly of chromatin on HSV DNA underlies the lytic versus latent decision of HSV. We propose a model for the decision to undergo a lytic or a latent infection in which HSV encodes gene products that modulate chromatin structure towards either euchromatin or heterochromatin, and we discuss the implications of this model for the development of therapeutics for HSV infections.

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Year:  2008        PMID: 18264117     DOI: 10.1038/nrmicro1794

Source DB:  PubMed          Journal:  Nat Rev Microbiol        ISSN: 1740-1526            Impact factor:   60.633


  232 in total

1.  Analysis of HSV Viral Reactivation in Explants of Sensory Neurons.

Authors:  Jesse H Arbuckle; Anne-Marie W Turner; Thomas M Kristie
Journal:  Curr Protoc Microbiol       Date:  2014-11-03

2.  HSV Recombinant Vectors for Gene Therapy.

Authors:  Roberto Manservigi; Rafaela Argnani; Peggy Marconi
Journal:  Open Virol J       Date:  2010-06-18

Review 3.  A hitchhiker's guide to the nervous system: the complex journey of viruses and toxins.

Authors:  Sara Salinas; Giampietro Schiavo; Eric J Kremer
Journal:  Nat Rev Microbiol       Date:  2010-09       Impact factor: 60.633

4.  Regulation of herpes simplex virus type 1 thymidine kinase gene expression by thyroid hormone receptor in cultured neuronal cells.

Authors:  Shao-Chung V Hsia; Rajeswara C Pinnoji; Gautam R Bedadala; James M Hill; Jayavardhana R Palem
Journal:  J Neurovirol       Date:  2010-02       Impact factor: 2.643

5.  Promoter-Targeted Histone Acetylation of Chromatinized Parvoviral Genome Is Essential for the Progress of Infection.

Authors:  Elina Mäntylä; Kari Salokas; Mikko Oittinen; Vesa Aho; Pekka Mäntysaari; Lassi Palmujoki; Olli Kalliolinna; Teemu O Ihalainen; Einari A Niskanen; Jussi Timonen; Keijo Viiri; Maija Vihinen-Ranta
Journal:  J Virol       Date:  2016-03-28       Impact factor: 5.103

6.  Therapeutic implications of new insights into the critical role of VP16 in initiating the earliest stages of HSV reactivation from latency.

Authors:  Richard L Thompson; Nancy M Sawtell
Journal:  Future Med Chem       Date:  2010-07       Impact factor: 3.808

7.  An Immortalized Human Dorsal Root Ganglion Cell Line Provides a Novel Context To Study Herpes Simplex Virus 1 Latency and Reactivation.

Authors:  Nikki M Thellman; Carolyn Botting; Zachary Madaj; Steven J Triezenberg
Journal:  J Virol       Date:  2017-05-26       Impact factor: 5.103

8.  Transcriptional Elongation of HSV Immediate Early Genes by the Super Elongation Complex Drives Lytic Infection and Reactivation from Latency.

Authors:  Roberto Alfonso-Dunn; Anne-Marie W Turner; Pierre M Jean Beltran; Jesse H Arbuckle; Hanna G Budayeva; Ileana M Cristea; Thomas M Kristie
Journal:  Cell Host Microbe       Date:  2017-04-12       Impact factor: 21.023

9.  TOP2β-Dependent Nuclear DNA Damage Shapes Extracellular Growth Factor Responses via Dynamic AKT Phosphorylation to Control Virus Latency.

Authors:  Hui-Lan Hu; Lora A Shiflett; Mariko Kobayashi; Moses V Chao; Angus C Wilson; Ian Mohr; Tony T Huang
Journal:  Mol Cell       Date:  2019-03-28       Impact factor: 17.970

10.  The rise of epigenetic targets for the development of novel antivirals.

Authors:  Thomas M Kristie
Journal:  Expert Rev Anti Infect Ther       Date:  2012-12       Impact factor: 5.091

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