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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: 30 September 2024 | Viewed by 1991

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

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

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

Published Papers (2 papers)

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Review

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
Viewed by 763
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 949
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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