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Viruses
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Regulation of the Virus Lifecycle by Cellular RNA-Binding Proteins
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Regulation of the Virus Lifecycle by Cellular RNA-Binding Proteins

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 (30 September 2024) | Viewed by 9621

Special Issue Editor

Dr. Alfredo Castello

E-Mail Website1 Website2
Guest Editor
Sir Michael Stoker Building, Garscube Campus, MRC University of Glasgow Centre for Virus Research, 464 Bearsden Road, Glasgow G61 1QH, UK
Interests: RNA binding proteins; RNA Virus; protein-RNA interactions; virus-host interactions; antivirals; interferon
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

RNA is a central molecule in the lifecycle of viruses, acting not only as messenger (m)RNA, but also as genome in the case of RNA viruses. Viruses dedicate a large proportion of their coding capacity to producing proteins that mediate the synthesis, processing, and regulation of the viral RNA. However, these proteins are insufficient to account for all the complex steps of the viral RNA lifecycle. Consequently, viruses rely on cellular RNA-binding proteins (RBPs), and these have been linked to virtually all the steps of virus infection, from replication to translation and packaging. Cellular RBPs are also critical in innate immunity. Viruses produce RNAs with abnormal signatures known as pathogen-associated molecular patterns (PAMPs). These include tri-phosphate ends, unmethylated cap structures, long double-stranded RNA and sequence biases and uncommon codons. These signatures are recognised by a set of specialised cellular RBPs that can function as sensors, triggering the antiviral defences, or effectors, repressing translation or inducing RNA degradation. Therefore, cellular RBPs are critical players in the host–virus battlefield, but the identity of the proteins engaging with viral RNA and the mechanisms underpinning their functions remain largely unknown. This Special Issue will explore these important host–virus interactions in order to advance our understanding of the viral life cycle and the antiviral defences of the host cell.

Dr. Alfredo Castello
Guest Editor

Manuscript Submission Information

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Keywords

  • RNA-binding proteins
  • RBPs protein–RNA interactions
  • antiviral defenses
  • viral life cycle

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Published Papers (5 papers)

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Research

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24 pages, 4534 KiB  
Article
The Polypyrimidine Tract-Binding Protein Is a Transacting Factor for the Dengue Virus Internal Ribosome Entry Site
by Leandro Fernández-García, Jenniffer Angulo and Marcelo López-Lastra
Viruses 2024, 16(11), 1757; https://doi.org/10.3390/v16111757 - 9 Nov 2024
Viewed by 1614
Abstract
Dengue virus (DENV) is an enveloped, positive sense, single-stranded RNA virus belonging to the Flaviviridae. Translation initiation of the DENV mRNA (vRNA) can occur following a cap-dependent, 5′-3’end-dependent internal ribosome entry site (IRES)-independent or IRES-dependent mechanism. This study evaluated the activity of [...] Read more.
Dengue virus (DENV) is an enveloped, positive sense, single-stranded RNA virus belonging to the Flaviviridae. Translation initiation of the DENV mRNA (vRNA) can occur following a cap-dependent, 5′-3’end-dependent internal ribosome entry site (IRES)-independent or IRES-dependent mechanism. This study evaluated the activity of DENV IRES in BHK-21 cells and the role of the polypyrimidine-tract binding protein (PTB) isoforms PTB1, PTB2, and PTB4 as IRES-transacting factors (ITAFs) for the DENV IRES. The results show that DENV-IRES activity is stimulated in DENV-replicating BHK-21 cells and cells expressing the Foot-and-mouth disease virus leader or Human rhinovirus 2A proteases. Protease activity was necessary, although a complete shutdown of cap-dependent translation initiation was not a requirement to stimulate DENV IRES activity. Regarding PTB, the results show that PTB1 > PTB2 > PTB4 stimulates DENV-IRES activity in BHK-21 cells. Mutations in the PTB RNA recognition motifs (RRMs), RRM1/RRM2 or RRM3/RRM4, differentially impact PTB1, PTB2, and PTB4’s ability to promote DENV IRES-mediated translation initiation in BHK-21 cells. PTB1-induced DENV-IRES stimulation is rescinded when RRM1/RRM2 or RRM3/RRM4 are disrupted. Mutations in RRM1/RRM2 or RRM3/RRM4 do not affect the ITAF activity of PTB2. Mutating RRM3/RRM4, but not RRM1/RRM2, abolishes the ability of PTB4 to stimulate the DENV IRES. Thus, PTB1, PTB2, and PTB4 are ITAFs for the DENV IRES. Full article
(This article belongs to the Special Issue Regulation of the Virus Lifecycle by Cellular RNA-Binding Proteins)
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Review

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27 pages, 1958 KiB  
Review
Host RNA-Binding Proteins as Regulators of HIV-1 Replication
by Sebastian Giraldo-Ocampo, Fernando Valiente-Echeverría and Ricardo Soto-Rifo
Viruses 2025, 17(1), 43; https://doi.org/10.3390/v17010043 - 31 Dec 2024
Viewed by 784
Abstract
RNA-binding proteins (RBPs) are cellular factors involved in every step of RNA metabolism. During HIV-1 infection, these proteins are key players in the fine-tuning of viral and host cellular and molecular pathways, including (but not limited to) viral entry, transcription, splicing, RNA modification, [...] Read more.
RNA-binding proteins (RBPs) are cellular factors involved in every step of RNA metabolism. During HIV-1 infection, these proteins are key players in the fine-tuning of viral and host cellular and molecular pathways, including (but not limited to) viral entry, transcription, splicing, RNA modification, translation, decay, assembly, and packaging, as well as the modulation of the antiviral response. Targeted studies have been of paramount importance in identifying and understanding the role of RNA-binding proteins that bind to HIV-1 RNAs. However, novel approaches aimed at identifying all the proteins bound to specific RNAs (RBPome), such as RNA interactome capture, have also contributed to expanding our understanding of the HIV-1 replication cycle, allowing the identification of RBPs with functions not only in viral RNA metabolism but also in cellular metabolism. Strikingly, several of the RBPs found through interactome capture are not canonical RBPs, meaning that they do not have conventional RNA-binding domains and are therefore not readily predicted as being RBPs. Further studies on the different cellular targets of HIV-1, such as subtypes of T cells or myeloid cells, or on the context (active replication versus reactivation from latency) are needed to fully elucidate the host RBPome bound to the viral RNA, which will allow researchers and clinicians to discover new therapeutic targets during active replication and provirus reactivation from latency. Full article
(This article belongs to the Special Issue Regulation of the Virus Lifecycle by Cellular RNA-Binding Proteins)
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17 pages, 2092 KiB  
Review
HPV and RNA Binding Proteins: What We Know and What Remains to Be Discovered
by Sheila V. Graham
Viruses 2024, 16(5), 783; https://doi.org/10.3390/v16050783 - 15 May 2024
Viewed by 1986
Abstract
Papillomavirus gene regulation is largely post-transcriptional due to overlapping open reading frames and the use of alternative polyadenylation and alternative splicing to produce the full suite of viral mRNAs. These processes are controlled by a wide range of cellular RNA binding proteins (RPBs), [...] Read more.
Papillomavirus gene regulation is largely post-transcriptional due to overlapping open reading frames and the use of alternative polyadenylation and alternative splicing to produce the full suite of viral mRNAs. These processes are controlled by a wide range of cellular RNA binding proteins (RPBs), including constitutive splicing factors and cleavage and polyadenylation machinery, but also factors that regulate these processes, for example, SR and hnRNP proteins. Like cellular RNAs, papillomavirus RNAs have been shown to bind many such proteins. The life cycle of papillomaviruses is intimately linked to differentiation of the epithelial tissues the virus infects. For example, viral late mRNAs and proteins are expressed only in the most differentiated epithelial layers to avoid recognition by the host immune response. Papillomavirus genome replication is linked to the DNA damage response and viral chromatin conformation, processes which also link to RNA processing. Challenges with respect to elucidating how RBPs regulate the viral life cycle include consideration of the orchestrated spatial aspect of viral gene expression in an infected epithelium and the epigenetic nature of the viral episomal genome. This review discusses RBPs that control viral gene expression, and how the connectivity of various nuclear processes might contribute to viral mRNA production. Full article
(This article belongs to the Special Issue Regulation of the Virus Lifecycle by Cellular RNA-Binding Proteins)
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14 pages, 1211 KiB  
Review
A Balancing Act: The Viral–Host Battle over RNA Binding Proteins
by Yahaira Bermudez, David Hatfield and Mandy Muller
Viruses 2024, 16(3), 474; https://doi.org/10.3390/v16030474 - 20 Mar 2024
Cited by 2 | Viewed by 2328
Abstract
A defining feature of a productive viral infection is the co-opting of host cell resources for viral replication. Despite the host repertoire of molecular functions and biological counter measures, viruses still subvert host defenses to take control of cellular factors such as RNA [...] Read more.
A defining feature of a productive viral infection is the co-opting of host cell resources for viral replication. Despite the host repertoire of molecular functions and biological counter measures, viruses still subvert host defenses to take control of cellular factors such as RNA binding proteins (RBPs). RBPs are involved in virtually all steps of mRNA life, forming ribonucleoprotein complexes (mRNPs) in a highly ordered and regulated process to control RNA fate and stability in the cell. As such, the hallmark of the viral takeover of a cell is the reshaping of RNA fate to modulate host gene expression and evade immune responses by altering RBP interactions. Here, we provide an extensive review of work in this area, particularly on the duality of the formation of RNP complexes that can be either pro- or antiviral. Overall, in this review, we highlight the various ways viruses co-opt RBPs to regulate RNA stability and modulate the outcome of infection by gathering novel insights gained from research studies in this field. Full article
(This article belongs to the Special Issue Regulation of the Virus Lifecycle by Cellular RNA-Binding Proteins)
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18 pages, 2234 KiB  
Review
Antiviral Defence Mechanisms during Early Mammalian Development
by Felix Mueller, Jeroen Witteveldt and Sara Macias
Viruses 2024, 16(2), 173; https://doi.org/10.3390/v16020173 - 24 Jan 2024
Cited by 1 | Viewed by 2233
Abstract
The type-I interferon (IFN) response constitutes the major innate immune pathway against viruses in mammals. Despite its critical importance for antiviral defence, this pathway is inactive during early embryonic development. There seems to be an incompatibility between the IFN response and pluripotency, the [...] Read more.
The type-I interferon (IFN) response constitutes the major innate immune pathway against viruses in mammals. Despite its critical importance for antiviral defence, this pathway is inactive during early embryonic development. There seems to be an incompatibility between the IFN response and pluripotency, the ability of embryonic cells to develop into any cell type of an adult organism. Instead, pluripotent cells employ alternative ways to defend against viruses that are typically associated with safeguard mechanisms against transposable elements. The absence of an inducible IFN response in pluripotent cells and the constitutive activation of the alternative antiviral pathways have led to the hypothesis that embryonic cells are highly resistant to viruses. However, some findings challenge this interpretation. We have performed a meta-analysis that suggests that the susceptibility of pluripotent cells to viruses is directly correlated with the presence of receptors or co-receptors for viral adhesion and entry. These results challenge the current view of pluripotent cells as intrinsically resistant to infections and raise the fundamental question of why these cells have sacrificed the major antiviral defence pathway if this renders them susceptible to viruses. Full article
(This article belongs to the Special Issue Regulation of the Virus Lifecycle by Cellular RNA-Binding Proteins)
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