[HTML][HTML] Herpesvirus latency

JI Cohen - The Journal of clinical investigation, 2020 - Am Soc Clin Investig
JI Cohen
The Journal of clinical investigation, 2020Am Soc Clin Investig
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 …
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.
The Journal of Clinical Investigation