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 706

Special Issue Editor


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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

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Keywords

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

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Published Papers (1 paper)

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Research

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 451
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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