Epigenetic and epitranscriptomic regulation of viral replication.

Journal Article (Journal Article;Review)

Eukaryotic gene expression is regulated not only by genomic enhancers and promoters, but also by covalent modifications added to both chromatin and RNAs. Whereas cellular gene expression may be either enhanced or inhibited by specific epigenetic modifications deposited on histones (in particular, histone H3), these epigenetic modifications can also repress viral gene expression, potentially functioning as a potent antiviral innate immune response in DNA virus-infected cells. However, viruses have evolved countermeasures that prevent the epigenetic silencing of their genes during lytic replication, and they can also take advantage of epigenetic silencing to establish latent infections. By contrast, the various covalent modifications added to RNAs, termed epitranscriptomic modifications, can positively regulate mRNA translation and/or stability, and both DNA and RNA viruses have evolved to utilize epitranscriptomic modifications as a means to maximize viral gene expression. As a consequence, both chromatin and RNA modifications could serve as novel targets for the development of antivirals. In this Review, we discuss how host epigenetic and epitranscriptomic processes regulate viral gene expression at the levels of chromatin and RNA function, respectively, and explore how viruses modify, avoid or utilize these processes in order to regulate viral gene expression.

Full Text

Duke Authors

Cited Authors

  • Tsai, K; Cullen, BR

Published Date

  • October 2020

Published In

Volume / Issue

  • 18 / 10

Start / End Page

  • 559 - 570

PubMed ID

  • 32533130

Pubmed Central ID

  • PMC7291935

Electronic International Standard Serial Number (EISSN)

  • 1740-1534

Digital Object Identifier (DOI)

  • 10.1038/s41579-020-0382-3


  • eng

Conference Location

  • England