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Viruses
Special Issues
Viral RNA and Its Interaction with the Host
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Viral RNA and Its Interaction with the Host

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "General Virology".

Deadline for manuscript submissions: 15 May 2026 | Viewed by 10123

Special Issue Editors

Dr. Redmond Smyth

E-Mail Website
Guest Editor
Helmholtz Institute for RNA-based Infection Research (HIRI), 97080 Würzburg, Germany
Interests: viruses; HIV; influenza; RNA; RNA structure; non-coding RNA; nucleic acids; evolution; next generation sequencing
Special Issues, Collections and Topics in MDPI journals
Dr. Neva Caliskan

E-Mail Website
Guest Editor
Helmholtz Institute for RNA-based Infection Research (HIRI), Helmholtz Centre for Infection Research (HZI), 97080 Würzburg, Germany
Interests: RNA molecules; virus; RNA-based therapeutics

Special Issue Information

Dear Colleague,

The life cycle of a virus is critically dependent on its ability to hijack the host cell’s machinery for its own replication and propagation. Central to this process is viral RNA. Not only does this carry the genetic information necessary for the synthesis of viral proteins, but it also contains RNA structural elements and non-coding sequences that are essential for regulating replication processes and host interactions. These non-coding elements can manipulate the host's protein synthesis machinery, alter immune responses, and control the spatiotemporal dynamics of viral assembly within the host cell.

This research topic aims to expand our mechanistic knowledge of viral RNA and its interactions with the host.

Potential topics:

Potential topics include, but are not limited to, the following:

-Importance of specific viral RNA structures during viral replication;
-Interactions between host or viral RNA binding proteins and viral RNA;
-Translational control by viral RNA;
-Role of RNA modifications in viral life cycles and pathogenicity;
-Immune recognition or evasion mediated by viral RNA;
-Viral RNA localization during infections

We welcome submissions of Original Research, Methods, Review, Mini-Review and Brief Research Report articles.

Dr. Redmond Smyth
Dr. Neva Caliskan
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

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

  • virus life cycle
  • host-virus interactions
  • viral RNA
  • RNA structures
  • RNA binding proteins
  • translational control
  • RNA modifications
  • immune evasion
  • RNA localization

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Published Papers (3 papers)

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Research

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12 pages, 1779 KB  
Article
Role of Unfolded Protein Response in the Apoptosis Induced by Alphaarterivirus: IRE1α as an Essential Pathway for In Vitro Replication
by Santiago Emanuel Colina, Macarena Marta Williman, María Soledad Serena, María Gabriela Echeverría and Germán Ernesto Metz
Viruses 2025, 17(10), 1301; https://doi.org/10.3390/v17101301 - 25 Sep 2025
Viewed by 610
Abstract
The perturbation of ER homeostasis by viral infection gives rise to the unfolded protein response (UPR), characterized by the activation of three signaling pathways. PERK, IRE1, and ATF6 have been identified as the primary mediators responsible for restoring homeostasis or leading to apoptosis [...] Read more.
The perturbation of ER homeostasis by viral infection gives rise to the unfolded protein response (UPR), characterized by the activation of three signaling pathways. PERK, IRE1, and ATF6 have been identified as the primary mediators responsible for restoring homeostasis or leading to apoptosis in response to stress. Alphaarterivirus equid, known as equine arteritis virus (EAV), is a RNA virus with importance in the equine industry that could persist in semen and lead to abortions in pregnant mares. The present article explores the consequences of in vitro infection with the EAV Bucyrus strain on UPR. Employing RT-PCR, qPCR and Western blot, our investigation has revealed the activation of PERK and IRE1α pathways, whilst ATF6 has been suppressed. Furthermore, the p38α MAPK, caspase-12, and CHOP genes were found to be upregulated, demonstrating the induction of apoptosis. Finally, in the inhibition experiments, the PERK pathway was found to be implicated in the modulation of viral replication in the initial phases of infection. Conversely, the IRE1α pathway was identified as the predominant UPR pathway in EAV replication, as evidenced by the complete inhibition of replication observed in these experiments. Consequently, the further exploration of this UPR pathway is necessary to determine whether it can effectively suppress EAV replication. Full article
(This article belongs to the Special Issue Viral RNA and Its Interaction with the Host)
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Review

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27 pages, 4043 KB  
Review
SARS-CoV-2 Spike Protein and Long COVID—Part 2: Understanding the Impact of Spike Protein and Cellular Receptor Interactions on the Pathophysiology of Long COVID Syndrome
by Bruno Pereira de Melo, Jhéssica Adriane Mello da Silva, Mariana Alves Rodrigues, Julys da Fonseca Palmeira, Angélica Amorim Amato, Gustavo Adolfo Argañaraz and Enrique Roberto Argañaraz
Viruses 2025, 17(5), 619; https://doi.org/10.3390/v17050619 - 25 Apr 2025
Cited by 1 | Viewed by 3888
Abstract
SARS-CoV-2 infection has had a significant impact on global health through both acute illness, referred to as coronavirus disease 2019 (COVID-19), and chronic conditions (long COVID or post-acute sequelae of COVID-19, PASC). Despite substantial advancements in preventing severe COVID-19 cases through vaccination, the [...] Read more.
SARS-CoV-2 infection has had a significant impact on global health through both acute illness, referred to as coronavirus disease 2019 (COVID-19), and chronic conditions (long COVID or post-acute sequelae of COVID-19, PASC). Despite substantial advancements in preventing severe COVID-19 cases through vaccination, the rise in the prevalence of long COVID syndrome and a notable degree of genomic mutation, primarily in the S protein, underscores the necessity for a deeper understanding of the underlying pathophysiological mechanisms related to the S protein of SARS-CoV-2. In this review, the latest part of this series, we investigate the potential pathophysiological molecular mechanisms triggered by the interaction between the spike protein and cellular receptors. Therefore, this review aims to provide a differential and focused view on the mechanisms potentially activated by the binding of the spike protein to canonical and non-canonical receptors for SARS-CoV-2, together with their possible interactions and effects on the pathogenesis of long COVID. Full article
(This article belongs to the Special Issue Viral RNA and Its Interaction with the Host)
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19 pages, 680 KB  
Review
SARS-CoV-2 Spike Protein and Long COVID—Part 1: Impact of Spike Protein in Pathophysiological Mechanisms of Long COVID Syndrome
by Bruno Pereira de Melo, Jhéssica Adriane Mello da Silva, Mariana Alves Rodrigues, Julys da Fonseca Palmeira, Felipe Saldanha-Araujo, Gustavo Adolfo Argañaraz and Enrique Roberto Argañaraz
Viruses 2025, 17(5), 617; https://doi.org/10.3390/v17050617 - 25 Apr 2025
Cited by 4 | Viewed by 5053
Abstract
SARS-CoV-2 infection has resulted in more than 700 million cases and nearly 7 million deaths worldwide. Although vaccination efforts have effectively reduced mortality and transmission rates, a significant proportion of recovered patients—up to 40%—develop long COVID syndrome (LC) or post-acute sequelae of COVID-19 [...] Read more.
SARS-CoV-2 infection has resulted in more than 700 million cases and nearly 7 million deaths worldwide. Although vaccination efforts have effectively reduced mortality and transmission rates, a significant proportion of recovered patients—up to 40%—develop long COVID syndrome (LC) or post-acute sequelae of COVID-19 infection (PASC). LC is characterized by the persistence or emergence of new symptoms following initial SARS-CoV-2 infection, affecting the cardiovascular, neurological, respiratory, gastrointestinal, reproductive, and immune systems. Despite the broad range of clinical symptoms that have been described, the risk factors and pathogenic mechanisms behind LC remain unclear. This review, the first of a two-part series, is distinguished by the discussion of the role of the SARS-CoV-2 spike protein in the primary mechanisms underlying the pathophysiology of LC. Full article
(This article belongs to the Special Issue Viral RNA and Its Interaction with the Host)
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