Review Series 10.1172/JCI136225
Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA.
Address correspondence to: Jeffrey I. Cohen, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, Building 50, Room 6134, 50 South Drive, MSC 8011, Bethesda, Maryland 20892, USA. Phone: 301.496.5265; Email: firstname.lastname@example.org.
First published May 4, 2020 - More info
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.
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