Epigenetics and the dynamics of chromatin during adenovirus infections

• Type of Material: Article
• Authors: Kelsey L. Lynch, Fred Hutchinson Cancer Center; Linda Gooding, Emory University; Charlie Garnett-Benson, Georgia State University; David A. Ornelles, Wake Forest University; Daphne C. Avgousti, Fred Hutchinson Cancer Center
• Language: English
• Date: 2019-12-15
• Publisher: WILEY
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2019 Federation of European Biochemical Societies
• Final Published Version (URL): http://dx.doi.org/10.1002/1873-3468.13697
• Title of Journal or Parent Work: FEBS LETTERS
• Volume: 593
• Issue: 24
• Start Page: 3551
• End Page: 3570
• Grant/Funding Information: Research in the Avgousti laboratory is supported by start-up funds from Fred Hutchinson Cancer Research Center and grants from the National Institutes of Health to DCA (GM133441), to KLL (CA9657), to DAO (CA127621) and to CG-B (CA162235).
• Keywords: TUMOR-SUPPRESSOR; E1A; post-translational modifications; DNA METHYLATION; POLYMERASE-CHAIN-REACTION; persistence; Life Sciences & Biomedicine; Cell Biology; CORE PROTEIN-VII; chromatin; Biophysics; epigenetics; TEMPLATE-ACTIVATING FACTOR; NUCLEOPROTEIN CORES; EARLY REGION-4; adenovirus; Biochemistry & Molecular Biology; host-pathogen interactions; E4ORF6 PROTEIN; histones; Science & Technology; HISTONE ACETYLATION; GENE-EXPRESSION; protein VII
• Research Categories: Chemistry, Biochemistry; Biophysics, Medical; Biology, Genetics; Biology, Cell

Abstract

The DNA genome of eukaryotic cells is compacted by histone proteins within the nucleus to form chromatin. Nuclear-replicating viruses such as adenovirus have evolved mechanisms of chromatin manipulation to promote infection and subvert host defenses. Epigenetic factors may also regulate persistent adenovirus infection and reactivation in lymphoid tissues. In this review, we discuss the viral proteins E1A and protein VII that interact with and alter host chromatin, as well as E4orf3, which separates host chromatin from sites of viral replication. We also highlight recent advances in chromatin technologies that offer new insights into virus-directed chromatin manipulation. Beyond the role of chromatin in the viral replication cycle, we discuss the nature of persistent viral genomes in lymphoid tissue and cell lines, and the potential contribution of epigenetic signals in maintaining adenovirus in a quiescent state. By understanding the mechanisms through which adenovirus manipulates host chromatin, we will understand new aspects of this ubiquitous virus and shed light on previously unknown aspects of chromatin biology.