Special Issue "Viral Interactions with Host RNA Decay Pathways"

A special issue of Viruses (ISSN 1999-4915).

Deadline for manuscript submissions: closed (15 September 2016).

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editors

Dr. J. Robert Hogg
Website
Guest Editor
National Heart, Lung, and Blood Institute, National Institutes of Health, 50 South Drive, Bethesda, MD 20892, USA
Interests: RNA decay; retroviral RNAs; RNA-protein interactions; translation; innate immunity
Prof. Dr. Karen L. Beemon
Website
Guest Editor
Department of Biology, The Johns Hopkins University, 3400 N. Charles Street, Baltimore, MD 21218, USA
Interests: Retroviruses; Rous sarcoma virus and avian leukosis virus; viral insertional mutagenesis; cancer biology; RNA splicing; nonsense-mediated RNA decay; microRNAs; lncRNAs

Special Issue Information

Dear Colleagues,

Eukaryotes have evolved a wide variety of RNA decay pathways to maintain cellular homeostasis, carry out programs of gene expression, and respond to changing environmental conditions. Individual RNA turnover mechanisms can operate constitutively or under only particular cellular conditions; similarly, some target many RNAs, while others act with great specificity. It has become increasingly clear that there are extensive interactions between viruses and the host RNA decay machinery. Often, the cellular RNA decay machinery poses a threat to viral gene expression, but viruses can also manipulate RNA decay pathways to promote viral replication. This special issue focuses on how cellular RNA decay factors recognize and degrade viral RNAs and viral strategies to subvert or evade these pathways.

Dr. J. Robert Hogg
Prof. Karen L. Beemon
Guest Editors

Manuscript Submission Information

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Keywords

  • RNA decay
  • RNA quality control
  • gene expression
  • translation
  • RNA-protein interactions

Published Papers (7 papers)

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Research

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Open AccessCommunication
Rous Sarcoma Virus RNA Stability Element Inhibits Deadenylation of mRNAs with Long 3′UTRs
Viruses 2017, 9(8), 204; https://doi.org/10.3390/v9080204 - 01 Aug 2017
Cited by 2
Abstract
All retroviruses use their full-length primary transcript as the major mRNA for Group-specific antigen (Gag) capsid proteins. This results in a long 3′ untranslated region (UTR) downstream of the termination codon. In the case of Rous sarcoma virus (RSV), there is a 7 [...] Read more.
All retroviruses use their full-length primary transcript as the major mRNA for Group-specific antigen (Gag) capsid proteins. This results in a long 3′ untranslated region (UTR) downstream of the termination codon. In the case of Rous sarcoma virus (RSV), there is a 7 kb 3′UTR downstream of the gag terminator, containing the pol, env, and src genes. mRNAs containing long 3′UTRs, like those with premature termination codons, are frequently recognized by the cellular nonsense-mediated mRNA decay (NMD) machinery and targeted for degradation. To prevent this, RSV has evolved an RNA stability element (RSE) in the RNA immediately downstream of the gag termination codon. This 400-nt RNA sequence stabilizes premature termination codons (PTCs) in gag. It also stabilizes globin mRNAs with long 3′UTRs, when placed downstream of the termination codon. It is not clear how the RSE stabilizes the mRNA and prevents decay. We show here that the presence of RSE inhibits deadenylation severely. In addition, the RSE also impairs decapping (DCP2) and 5′-3′ exonucleolytic (XRN1) function in knockdown experiments in human cells. Full article
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Review

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Open AccessReview
Virus Escape and Manipulation of Cellular Nonsense-Mediated mRNA Decay
Viruses 2017, 9(1), 24; https://doi.org/10.3390/v9010024 - 23 Jan 2017
Cited by 19
Abstract
Nonsense-mediated mRNA decay (NMD), a cellular RNA turnover pathway targeting RNAs with features resulting in aberrant translation termination, has recently been found to restrict the replication of positive-stranded RNA ((+)RNA) viruses. As for every other antiviral immune system, there is also evidence of [...] Read more.
Nonsense-mediated mRNA decay (NMD), a cellular RNA turnover pathway targeting RNAs with features resulting in aberrant translation termination, has recently been found to restrict the replication of positive-stranded RNA ((+)RNA) viruses. As for every other antiviral immune system, there is also evidence of viruses interfering with and modulating NMD to their own advantage. This review will discuss our current understanding of why and how NMD targets viral RNAs, and elaborate counter-defense strategies viruses utilize to escape NMD. Full article
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Open AccessReview
Attacked from All Sides: RNA Decay in Antiviral Defense
Viruses 2017, 9(1), 2; https://doi.org/10.3390/v9010002 - 04 Jan 2017
Cited by 21
Abstract
The innate immune system has evolved a number of sensors that recognize viral RNA (vRNA) to restrict infection, yet the full spectrum of host-encoded RNA binding proteins that target these foreign RNAs is still unknown. The RNA decay machinery, which uses exonucleases to [...] Read more.
The innate immune system has evolved a number of sensors that recognize viral RNA (vRNA) to restrict infection, yet the full spectrum of host-encoded RNA binding proteins that target these foreign RNAs is still unknown. The RNA decay machinery, which uses exonucleases to degrade aberrant RNAs largely from the 5′ or 3′ end, is increasingly recognized as playing an important role in antiviral defense. The 5′ degradation pathway can directly target viral messenger RNA (mRNA) for degradation, as well as indirectly attenuate replication by limiting specific pools of endogenous RNAs. The 3′ degradation machinery (RNA exosome) is emerging as a downstream effector of a diverse array of vRNA sensors. This review discusses our current understanding of the roles of the RNA decay machinery in controlling viral infection. Full article
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Open AccessReview
Use of Cellular Decapping Activators by Positive-Strand RNA Viruses
Viruses 2016, 8(12), 340; https://doi.org/10.3390/v8120340 - 21 Dec 2016
Cited by 5
Abstract
Positive-strand RNA viruses have evolved multiple strategies to not only circumvent the hostile decay machinery but to trick it into being a priceless collaborator supporting viral RNA translation and replication. In this review, we describe the versatile interaction of positive-strand RNA viruses and [...] Read more.
Positive-strand RNA viruses have evolved multiple strategies to not only circumvent the hostile decay machinery but to trick it into being a priceless collaborator supporting viral RNA translation and replication. In this review, we describe the versatile interaction of positive-strand RNA viruses and the 5′-3′ mRNA decay machinery with a focus on the viral subversion of decapping activators. This highly conserved viral trickery is exemplified with the plant Brome mosaic virus, the animal Flock house virus and the human hepatitis C virus. Full article
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Open AccessReview
Diverse Strategies Used by Picornaviruses to Escape Host RNA Decay Pathways
Viruses 2016, 8(12), 335; https://doi.org/10.3390/v8120335 - 20 Dec 2016
Cited by 9
Abstract
To successfully replicate, viruses protect their genomic material from degradation by the host cell. RNA viruses must contend with numerous destabilizing host cell processes including mRNA decay pathways and viral RNA (vRNA) degradation resulting from the antiviral response. Members of the Picornaviridae family [...] Read more.
To successfully replicate, viruses protect their genomic material from degradation by the host cell. RNA viruses must contend with numerous destabilizing host cell processes including mRNA decay pathways and viral RNA (vRNA) degradation resulting from the antiviral response. Members of the Picornaviridae family of small RNA viruses have evolved numerous diverse strategies to evade RNA decay, including incorporation of stabilizing elements into vRNA and re-purposing host stability factors. Viral proteins are deployed to disrupt and inhibit components of the decay machinery and to redirect decay machinery to the advantage of the virus. This review summarizes documented interactions of picornaviruses with cellular RNA decay pathways and processes. Full article
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Open AccessReview
Interactions between the HIV-1 Unspliced mRNA and Host mRNA Decay Machineries
Viruses 2016, 8(11), 320; https://doi.org/10.3390/v8110320 - 23 Nov 2016
Cited by 8
Abstract
The human immunodeficiency virus type-1 (HIV-1) unspliced transcript is used both as mRNA for the synthesis of structural proteins and as the packaged genome. Given the presence of retained introns and instability AU-rich sequences, this viral transcript is normally retained and degraded in [...] Read more.
The human immunodeficiency virus type-1 (HIV-1) unspliced transcript is used both as mRNA for the synthesis of structural proteins and as the packaged genome. Given the presence of retained introns and instability AU-rich sequences, this viral transcript is normally retained and degraded in the nucleus of host cells unless the viral protein REV is present. As such, the stability of the HIV-1 unspliced mRNA must be particularly controlled in the nucleus and the cytoplasm in order to ensure proper levels of this viral mRNA for translation and viral particle formation. During its journey, the HIV-1 unspliced mRNA assembles into highly specific messenger ribonucleoproteins (mRNPs) containing many different host proteins, amongst which are well-known regulators of cytoplasmic mRNA decay pathways such as up-frameshift suppressor 1 homolog (UPF1), Staufen double-stranded RNA binding protein 1/2 (STAU1/2), or components of miRNA-induced silencing complex (miRISC) and processing bodies (PBs). More recently, the HIV-1 unspliced mRNA was shown to contain N6-methyladenosine (m6A), allowing the recruitment of YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), an m6A reader host protein involved in mRNA decay. Interestingly, these host proteins involved in mRNA decay were shown to play positive roles in viral gene expression and viral particle assembly, suggesting that HIV-1 interacts with mRNA decay components to successfully accomplish viral replication. This review summarizes the state of the art in terms of the interactions between HIV-1 unspliced mRNA and components of different host mRNA decay machineries. Full article
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Open AccessReview
Gene Regulation and Quality Control in Murine Polyomavirus Infection
Viruses 2016, 8(10), 284; https://doi.org/10.3390/v8100284 - 17 Oct 2016
Cited by 3
Abstract
Murine polyomavirus (MPyV) infects mouse cells and is highly oncogenic in immunocompromised hosts and in other rodents. Its genome is a small, circular DNA molecule of just over 5000 base pairs and it encodes only seven polypeptides. While seemingly simply organized, this virus [...] Read more.
Murine polyomavirus (MPyV) infects mouse cells and is highly oncogenic in immunocompromised hosts and in other rodents. Its genome is a small, circular DNA molecule of just over 5000 base pairs and it encodes only seven polypeptides. While seemingly simply organized, this virus has adopted an unusual genome structure and some unusual uses of cellular quality control pathways that, together, allow an amazingly complex and varied pattern of gene regulation. In this review we discuss how MPyV leverages these various pathways to control its life cycle. Full article
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