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Viruses
Special Issues
Viruses, MicroRNAs and Host Interactions
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Viruses, MicroRNAs and Host Interactions

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 1856

Special Issue Editor

Prof. Dr. John Paul Pezacki

E-Mail Website
Guest Editor
Department of Chemistry and Biomolecular Sciences, University of Ottawa, Ottawa, ON K1N 6N5, Canada
Interests: RNA viruses; HCV; SARS-CoV-2; DENV; innate immunity; chemical biology; genetic code expansion; antivirals

Special Issue Information

Dear Colleagues,

Viruses have the ability to interact directly or indirectly with host cell microRNAs (miRNAs) or even encode for their own miRNAs. The effects on target mRNA expression can affect pathways that are either pro- or antiviral and help viruses alter their host cells in favour of viral pathogenesis. These interactions ultimately have the potential to impact virus-induced disease progression. For example, miRNAs may upregulate metabolic processes that help provide essential building blocks for viral replication, or may be involved in immune evasion thereby enhancing viral persistence. miRNAs have even been shown to interact directly with viral genomes and protect viral genomic RNA. This Special Issue examines current knowledge and new developments in the study of microRNAs, viruses, and their host interactions.

Prof. Dr. John Paul Pezacki
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • microRNA
  • RNA–protein interactions
  • host factor
  • mRNA silencing

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Published Papers (2 papers)

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Research

16 pages, 1907 KiB  
Article
Characterizing Host microRNA: Virus Interactions of Orthoavulavirus javaense
by Megan C. Mears and Abhijeet Bakre
Viruses 2024, 16(11), 1748; https://doi.org/10.3390/v16111748 - 7 Nov 2024
Viewed by 667
Abstract
Post-transcriptional gene regulation mediated by microRNAs (miRNAs) relies on sequence complementarity between the miRNA seed site and the target gene transcript(s). This complementarity can completely inhibit or reduce translation into protein. We hypothesized that viruses employ sequence complementarity/similarity with host miRNAs to inhibit [...] Read more.
Post-transcriptional gene regulation mediated by microRNAs (miRNAs) relies on sequence complementarity between the miRNA seed site and the target gene transcript(s). This complementarity can completely inhibit or reduce translation into protein. We hypothesized that viruses employ sequence complementarity/similarity with host miRNAs to inhibit or increase the miRNA-mediated regulation of host gene expression specifically during viral infection(s). In this study, we focus on Orthoavulavirus javaense (OAVJ), the causative of Newcastle disease, a poultry disease with significant economic impact. A computational analysis of OAVJ genomes from low-virulence (lentogenic) versus virulent (velogenic) viruses was carried out to identify viral signature motifs that potentially either mimic or complement host miRNA seed sequences. Data show that OAVJ genomes harbor viral seed mimics (vSMs) or viral seed sponges (vSSs) and can mimic host miRNAs or inhibit their regulation of host genes, disrupting cellular pathways. Our analyses showed that velogens encode a statistically significant higher number of vSMs and a lower number of vSSs relative to lentogens. The number of vSMs or vSSs did not correlate with gene length. The analysis of the secondary structures flanking these vSMs and vSSs showed structural features common to miRNA precursors. The inhibition or upregulation of vSS-miR-27b-5p altered P gene expression in a sequence-dependent manner. These data demonstrate that viral transcripts can interact with host miRNAs to alter the outcomes of infection. Full article
(This article belongs to the Special Issue Viruses, MicroRNAs and Host Interactions)
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18 pages, 2688 KiB  
Article
Poly(rC)-Binding Protein 2 Does Not Directly Participate in HCV Translation or Replication, but Rather Modulates Genome Packaging
by Sophie E. Cousineau, Carolina Camargo and Selena M. Sagan
Viruses 2024, 16(8), 1220; https://doi.org/10.3390/v16081220 - 30 Jul 2024
Viewed by 851
Abstract
The hepatitis C virus (HCV) co-opts many cellular factors—including proteins and microRNAs—to complete its life cycle. A cellular RNA-binding protein, poly(rC)-binding protein 2 (PCBP2), was previously shown to bind to the hepatitis C virus (HCV) genome; however, its precise role in the viral [...] Read more.
The hepatitis C virus (HCV) co-opts many cellular factors—including proteins and microRNAs—to complete its life cycle. A cellular RNA-binding protein, poly(rC)-binding protein 2 (PCBP2), was previously shown to bind to the hepatitis C virus (HCV) genome; however, its precise role in the viral life cycle remained unclear. Herein, using the HCV cell culture (HCVcc) system and assays that isolate each step of the viral life cycle, we found that PCBP2 does not have a direct role in viral entry, translation, genome stability, or HCV RNA replication. Rather, our data suggest that PCBP2 depletion only impacts viral RNAs that can undergo genome packaging. Taken together, our data suggest that endogenous PCBP2 modulates the early steps of genome packaging, and therefore only has an indirect effect on viral translation and RNA replication, likely by increasing the translating/replicating pool of viral RNAs to the detriment of virion assembly. Full article
(This article belongs to the Special Issue Viruses, MicroRNAs and Host Interactions)
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