Viral Strategies and Cellular Countermeasures That Regulate mRNA Access to the Translation Apparatus: 2nd Edition

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

Deadline for manuscript submissions: 31 December 2025 | Viewed by 921

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Department of Cell Biology, State University of New York Downstate Health Sciences University, Brooklyn, NY 11203, USA
Interests: eukaryotic translation mechanisms and their exploitation by viruses
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Dear Colleagues,

Viruses depend on the translation apparatus of host cells for the synthesis of viral proteins. Infection is consequently influenced by competition between viral mechanisms that act to co-opt the cellular translation apparatus and cellular mechanisms that restrict viral access to it. Viral strategies include (a) synthesis of proteins that substitute for specific components of the translation apparatus, (b) modification of components of the host translation apparatus such as translation factors, ribosomes, or host mRNAs, thereby restricting cellular translation and the execution of cellular antiviral responses, and (c) exploitation of specialized elements in viral mRNAs to enable them to access the translation apparatus in these conditions. Viral infection imposes stresses on cells that activate signaling pathways and host innate immune defenses that may specifically silence translation of viral mRNAs or lead to a global shut-down of translation. Viruses have, in turn, evolved mechanisms to evade or subvert these host responses, thereby enabling viral translation to be maintained during infection.

This Special Issue will focus on recent advances in identifying viral effects on the cellular translation apparatus, in characterizing specialized viral translation mechanisms that function during infection, and in elucidating details of cellular mechanisms that restrict viral translation.

Dr. Christopher Hellen
Guest Editor

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Keywords

  • virus–host interactions
  • IRES elements
  • RNA structure
  • translation initiation
  • translational control
  • innate immune response
  • RNA modification

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Research

16 pages, 5856 KiB  
Article
Characterization of Gene Expression Suppression by Bovine Coronavirus Non-Structural Protein 1
by Takehiro Ohkami, Ichika Kitashin, Riko Kawashima, Aimi Yoshida, Taizo Saito, Yasuhiro Takashima, Wataru Kamitani and Keisuke Nakagawa
Viruses 2025, 17(7), 978; https://doi.org/10.3390/v17070978 - 13 Jul 2025
Viewed by 231
Abstract
Coronavirus non-structural protein 1 (nsp1) is a pathogenic determinant of Betacoronaviruses. Previous studies demonstrated that the nsp1 of various coronaviruses induces host shutoff through a variety of mechanisms; however, there is little information on the function of bovine coronavirus (BCoV) nsp1. We [...] Read more.
Coronavirus non-structural protein 1 (nsp1) is a pathogenic determinant of Betacoronaviruses. Previous studies demonstrated that the nsp1 of various coronaviruses induces host shutoff through a variety of mechanisms; however, there is little information on the function of bovine coronavirus (BCoV) nsp1. We aimed to characterize the host gene expression suppression function of BCoV nsp1. We first confirmed that the expression of BCoV nsp1 in MAC-T cells, a bovine mammary epithelial cell line, suppressed host and reporter gene expression. Subsequently, lysine and phenylalanine at amino acid positions 232 and 233, respectively, were identified as key residues required for this suppressive effect. Expression levels of housekeeping genes are comparable in cells expressing wild-type BCoV nsp1 and a mutant with alanine substitutions at positions 232 and 233 (BCoV nsp1-KF). Wild-type BCoV nsp1 localized to both the cytoplasm and nucleus; however, BCoV nsp1-KF exhibited prominent nuclear accumulation with dot-like structures. Using confocal microscopy and co-sedimentation analysis, we identified an association between wild-type BCoV nsp1, but not BCoV nsp1-KF, and ribosomes, suggesting that ribosome binding is required for BCoV nsp1-mediated suppression of host gene expression. This is the first study of the characterization of host gene expression suppression by BCoV nsp1. Full article
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