Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Aging (Upcoming)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • Gut-Brain Axis (Jul 2021)
    • Tumor Microenvironment (Mar 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Herpesvirus latency
Jeffrey I. Cohen
Jeffrey I. Cohen
Published May 4, 2020
Citation Information: J Clin Invest. 2020;130(7):3361-3369. https://doi.org/10.1172/JCI136225.
View: Text | PDF
Review Series

Herpesvirus latency

  • Text
  • PDF
Abstract

Herpesviruses infect virtually all humans and establish lifelong latency and reactivate to infect other humans. Latency requires multiple functions: maintaining the herpesvirus genome in the nuclei of cells; partitioning the viral genome to daughter cells in dividing cells; avoiding recognition by the immune system by limiting protein expression; producing noncoding viral RNAs (including microRNAs) to suppress lytic gene expression or regulate cellular protein expression that could otherwise eliminate virus-infected cells; modulating the epigenetic state of the viral genome to regulate viral gene expression; and reactivating to infect other hosts. Licensed antivirals inhibit virus replication, but do not affect latency. Understanding of the mechanisms of latency is leading to novel approaches to destroy latently infected cells or inhibit reactivation from latency.

Authors

Jeffrey I. Cohen

×

Figure 1

Features of herpesvirus latency.

Options: View larger image (or click on image) Download as PowerPoint
Features of herpesvirus latency.
(A and B) Latent herpesvirus genomes ar...
(A and B) Latent herpesvirus genomes are maintained in the nuclei of cells as circular episomes (A) and in dividing cells the viruses express proteins during cell division that partition the episomes to daughter cells (B). (C) Alphaherpesviruses encode long noncoding viral RNAs during latency that are transcribed antisense to viral genes expressed during lytic infection. (D) Latent herpesvirus DNA genomes are associated with histone proteins; genes normally expressed during virus lytic replication are silenced by methylation or other modifications of their histone tails during latency. (E) Chromatin insulators containing DNA sequences and the corresponding DNA-binding proteins and chromatin-modifying proteins act to separate regions of active euchromatin and repressed heterochromatin to regulate latency. (F) Herpesvirus microRNAs (miRNAs) produced during latency degrade or inhibit expression of virus lytic genes or host cell genes.

Copyright © 2022 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts