New Insights in Viral Diseases and Computational Biology

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 1172

Special Issue Editor


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Guest Editor
Institute of Infection, Veterinary and Ecological Sciences, University of Liverpool, IC2 Building, Liverpool L3 5RF, UK
Interests: bioinformatics; virus evolution; host transcriptome; mutation; machine learning

Special Issue Information

Dear Colleagues,

Humanity and animality are facing threats from various viruses, including RNA viruses such as SARS-CoV-2, the influenza virus, the respiratory syncytial virus (RSV), and the Ebola virus. SARS-CoV-2, influenza virus, and respiratory syncytial virus all cause acute respiratory viral infections. As of August 2023, the World Health Organization (WHO) had reported over 769 million confirmed cases of COVID-19 and approximately 6.95 million confirmed deaths. The overlap of SARS-CoV-2 with seasonal epidemics of RSV and influenza viruses has also resulted in significant morbidity and mortality among young children worldwide [1]. Although Ebola virus outbreaks have been mainly restricted to Africa, they have resulted in much higher fatality rates, with an average of around 50%.

Bioinformatics approaches, employing vast new technologies, have been widely used to address research questions regarding virus evolution and host responses. Second- and third-generation sequencing have provided large amounts of resource data for bioinformatics analysis, aiding in the understanding of the biology of both the virus and its infected host.

In the form of a Special Issue, our aim is to provide a collection of the most recent top research articles, comprehensive reviews, as well as short communications in line with computational virus biology. Through this Special Issue, we aim to pinpoint our efforts towards understanding the infection biology of viruses using various bioinformatics approaches.

I am looking forward to your valuable involvement in this interesting Special Issue.

Reference:

1. Steponavičienė, A.; Burokienė, S.; Ivaškevičienė, I.; Stacevičienė, I.; Vaičiūnienė, D.; Jankauskienė, A. Influenza and Respiratory Syncytial Virus Infections in Pediatric Patients during the COVID-19 Pandemic: A Single-Center Experience. Children 2023, 10, 126.

Dr. Xiaofeng Dong
Guest Editor

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Keywords

  • bioinformatics method/pipeline in virology
  • virus genome evolution
  • host transcriptome
  • virus and host interaction
  • bioinformatics in the design of antiviral drug and vaccines
  • machine learning in virology

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Published Papers (1 paper)

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Research

23 pages, 5143 KiB  
Article
Modular Polymerase Synthesis and Internal Protein Domain Swapping via Dual Opposed Frameshifts in the Ebola Virus L Gene
by David B. Stubbs, Jan A. Ruzicka and Ethan W. Taylor
Pathogens 2024, 13(10), 829; https://doi.org/10.3390/pathogens13100829 - 25 Sep 2024
Viewed by 855
Abstract
Sequence analysis of the Zaire ebolavirus (EBOV) polymerase (L gene) mRNA, using online tools, identified a highly ranked −1 programmed ribosomal frameshift (FS) signal including an ideal slippery sequence heptamer (UUUAAAA), with an overlapping coding region featuring two tandem UGA codons, immediately followed [...] Read more.
Sequence analysis of the Zaire ebolavirus (EBOV) polymerase (L gene) mRNA, using online tools, identified a highly ranked −1 programmed ribosomal frameshift (FS) signal including an ideal slippery sequence heptamer (UUUAAAA), with an overlapping coding region featuring two tandem UGA codons, immediately followed by an RNA region that is the inverse complement (antisense) to a region of the mRNA of the selenoprotein iodothyronine deiodinase II (DIO2). This antisense interaction was confirmed in vitro via electrophoretic gel shift assay, using cDNAs at the EBOV and DIO2 segments. The formation of a duplex between the two mRNAs could trigger the ribosomal frameshift, by mimicking the enhancing role of a pseudoknot structure, while providing access to the selenocysteine insertion sequence (SECIS) element contained in the DIO2 mRNA. This process would allow the −1 frame UGA codons to be recoded as selenocysteine, forming part of a C-terminal module in a low abundance truncated isoform of the viral polymerase, potentially functioning in a redox role. Remarkably, 90 bases downstream of the −1 FS site, an active +1 FS site can be demonstrated, which, via a return to the zero frame, would enable the attachment of the entire C-terminal of the polymerase protein. Using a construct with upstream and downstream reporter genes, spanning a wildtype or mutated viral insert, we show significant +1 ribosomal frameshifting at this site. Acting singly or together, frameshifting at these sites (both of which are highly conserved in EBOV strains) could enable the expression of several modified isoforms of the polymerase. The 3D modeling of the predicted EBOV polymerase FS variants using the AI tool, AlphaFold, reveals a peroxiredoxin-like active site with arginine and threonine residues adjacent to a putative UGA-encoded selenocysteine, located on the back of the polymerase “hand”. This module could serve to protect the viral RNA from peroxidative damage. Full article
(This article belongs to the Special Issue New Insights in Viral Diseases and Computational Biology)
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