| Literature DB >> 31769503 |
Kelsey L Lynch1, Linda R Gooding2, Charlie Garnett-Benson3, David A Ornelles4, Daphne C Avgousti1.
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.Entities:
Keywords: E1A; adenovirus; chromatin; epigenetics; histones; host-pathogen interactions; persistence; post-translational modifications; protein VII
Mesh:
Substances:
Year: 2019 PMID: 31769503 PMCID: PMC6938402 DOI: 10.1002/1873-3468.13697
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124