MicroRNA Regulation of Human Herpesvirus Latency

Herpesviruses are ubiquitous human pathogens. After productive (lytic) infection, all human herpesviruses are able to establish life-long latent infection and reactivate from it. Latent infection entails suppression of viral replication, maintenance of the viral genome in infected cells, and the ability to reactivate. Most human herpesviruses encode microRNAs (miRNAs) that regulate these processes during latency. Meanwhile, cellular miRNAs are hijacked by herpesviruses to participate in these processes. The viral or cellular miRNAs either directly target viral transcripts or indirectly affect viral infection through host pathways. These findings shed light on the molecular determinants that control the lytic-latent switch and may lead to novel therapeutics targeting latent infection. We discuss the multiple mechanisms by which miRNAs regulate herpesvirus latency, focusing on the patterns in these mechanisms.

Automated summary

Herpesviruses are commonly found human pathogens that have the ability to establish latent infection and reactivate. Both viral and cellular microRNAs play a critical role in regulating the latency process. These findings are significant for understanding the mechanisms of viral replication and latency switch, as well as for developing novel therapeutics.