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      Herpes Simplex Virus 1 Deregulation of Host MicroRNAs

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          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.

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          Origins and Mechanisms of miRNAs and siRNAs.

          Richard W. Carthew, Erik J. Sontheimer (2009)
          Over the last decade, approximately 20-30 nucleotide RNA molecules have emerged as critical regulators in the expression and function of eukaryotic genomes. Two primary categories of these small RNAs--short interfering RNAs (siRNAs) and microRNAs (miRNAs)--act in both somatic and germline lineages in a broad range of eukaryotic species to regulate endogenous genes and to defend the genome from invasive nucleic acids. Recent advances have revealed unexpected diversity in their biogenesis pathways and the regulatory mechanisms that they access. Our understanding of siRNA- and miRNA-based regulation has direct implications for fundamental biology as well as disease etiology and treatment.
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            MicroRNA (miRNA) transcriptome of mouse retina and identification of a sensory organ-specific miRNA cluster.

            Shunbin Xu, P Dane Witmer, Stephen Lumayag … (2007)
            Although microRNAs (miRNAs) provide a newly recognized level of regulation of gene expression, the miRNA transcriptome of the retina and the contributions of miRNAs to retinal development and function are largely unknown. To begin to understand the functions of miRNAs in retina, we compared miRNA expression profiles in adult mouse retina, brain, and heart by microarray analysis. Our results show that at least 78 miRNAs are expressed in adult mouse retina, 21 of which are potentially retina-specific. Among these, we identified a polycistronic, sensory organ-specific paralogous miRNA cluster that includes miR-96, miR-182, and miR-183 on mouse chromosome 6qA3 with conservation of synteny to human chromosome 7q32.2. In situ hybridization showed that members of this cluster are expressed in photoreceptors, retinal bipolar and amacrine cells. Consistent with their genomic organization, these miRNAs have a similar expression pattern during development with abundance increasing postnatally and peaking in adult retina. Target prediction and in vitro functional studies showed that MITF, a transcription factor required for the establishment and maintenance of retinal pigmented epithelium, is a direct target of miR-96 and miR-182. Additionally, to identify miRNAs potentially involved in circadian rhythm regulation of the retina, we performed miRNA expression profiling with retinal RNA harvested at noon (Zeitgeber time 5) and midnight (Zeitgeber time 17) and identified a subgroup of 12 miRNAs, including members of the miR-183/96/182 cluster with diurnal variation in expression pattern. Our results suggest that miR-96 and miR-182 are involved in circadian rhythm regulation, perhaps by modulating the expression of adenylyl cyclase VI (ADCY6).
            Article 0 comments Cited 186 times – based on 0 reviews     Review now
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              Making RISC.

              Tomoko Kawamata, Yukihide Tomari (2010)
              It is well established that 20- to 30-nt small RNAs, including small interfering RNAs, microRNAs and Piwi-interacting RNAs, play crucial roles in regulating gene expression and control a surprisingly diverse array of biological processes. These small RNAs cannot work alone: they must form effector ribonucleoprotein complexes - RNA-induced silencing complexes (RISCs) - to exert their function. Thus, RISC assembly is a key process in small RNA-mediated silencing. Recent biochemical analyses of RISC assembly, together with new structural studies of Argonaute, the core protein component of RISC, suggest a revised view of how mature RISC, which contains single-stranded guide RNA, is built from small RNAs that are born double-stranded. Copyright 2010 Elsevier Ltd. All rights reserved.
              Article 0 comments Cited 174 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Noncoding RNA
                Journal ID (iso-abbrev): Noncoding RNA
                Journal ID (publisher-id): ncrna
                Title: Non-Coding RNA
                Publisher: MDPI
                ISSN (Electronic): 2311-553X
                Publication date (Electronic): 23 November 2018
                Publication date Collection: December 2018
                Volume: 4
                Issue: 4
                Electronic Location Identifier: 36
                Affiliations
                Laboratory for Molecular Virology, Department of Biotechnology, University of Rijeka, R. Matejčić 2, HR-51000 Rijeka, Croatia; maja.cokaric@ 123456biotech.uniri.hr (M.C.B.); azubkovic@ 123456biotech.uniri.hr (A.Z.)
                Author notes
                [* ]Correspondence: igor.jurak@ 123456biotech.uniri.hr ; Tel.: +385-51-584-580
                Author information
                https://orcid.org/0000-0002-9335-8700
                https://orcid.org/0000-0002-7271-2643
                Article
                Publisher ID: ncrna-04-00036
                DOI: 10.3390/ncrna4040036
                PMC ID: 6316616
                PubMed ID: 30477082
                SO-VID: a603c6e4-122b-4c1c-abe2-47ba75171e29
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 24 October 2018
                Date accepted : 19 November 2018
                Categories
                Subject: Review

                Keywords: mirnas,host–pathogen interaction,hsv-1,latency,productive replication,antiviral innate immune response,apoptosis
                Data availability:
                Keywords: mirnas, host–pathogen interaction, hsv-1, latency, productive replication, antiviral innate immune response, apoptosis

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