Abstract
Viruses utilize microRNAs (miRNAs) in a vast variety of possible interactions and mechanisms, apparently far beyond the classical understanding of gene repression in humans. Likewise, herpes simplex virus 1 (HSV-1) expresses numerous miRNAs and deregulates the expression of host miRNAs. Several HSV-1 miRNAs are abundantly expressed in latency, some of which are encoded antisense to transcripts of important productive infection genes, indicating their roles in repressing the productive cycle and/or in maintenance/reactivation from latency. In addition, HSV-1 also exploits host miRNAs to advance its replication or repress its genes to facilitate latency. Here, we discuss what is known about the functional interplay between HSV-1 and the host miRNA machinery, potential targets, and the molecular mechanisms leading to an efficient virus replication and spread.
Highlights
Throughout millions of years of co-evolution with their hosts, viruses have been successfully avoiding defense mechanisms and, at the same time, hijacking and harvesting the products of the host’s metabolism to thrive
The negative regulation of virus gene products is counterintuitive from the perspective of virus replication, there are many studies showing that the main role of latent viruses encoding miRNAs (vmiRNAs) is to limit the expression of gene products that are important for the productive infection and preventing host defense mechanisms [9,10] to facilitate the establishment of latency and further spread
We briefly summarize the biology of Herpes simplex virus 1 (HSV-1), a prototype of α-herpesviruses, and the current understanding of herpes simplex virus 1 (HSV-1)-encoded miRNAs and their functions
Summary
Throughout millions of years of co-evolution with their hosts, viruses have been successfully avoiding defense mechanisms and, at the same time, hijacking and harvesting the products of the host’s metabolism to thrive. The negative regulation of virus gene products is counterintuitive from the perspective of virus replication, there are many studies showing that the main role of latent vmiRNAs is to limit the expression of gene products that are important for the productive infection (e.g., virus-encoded trans-activators of gene expression) and preventing host defense mechanisms [9,10] to facilitate the establishment of latency and further spread. In contrast to direct pairing of host miRNAs with viral genomes or transcripts, there are numerous studies showing that viruses can dramatically alter the miRNAome of the infected cells, deregulating cellular factors involved in host defense, control of cell death, and virulence (reviewed in [20]), some of which are described below. We discuss experimental challenges in addressing the functions of miRNAs in HSV-1 infection and perspectives for further research in the field
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