Special Issue "Translational Control at the Virus–Host Interface"

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

Deadline for manuscript submissions: closed (28 February 2021).

Special Issue Editor

Prof. Nicolas Locker
E-Mail Website
Guest Editor
University of Surrey, Guildford, Surrey GU2 7XH, UK
Interests: viruses; translational control; RNA biology; stress responses; membraneless organelles

Special Issue Information

Dear Colleagues,

The synthesis of viral proteins, whose functions include genome replication, evasion of immune defenses, and virion biogenesis, is wholly dependent on host cell translation machinery. However, during infection, the accumulation of RNA replication intermediates or viral proteins imposes major stress on the host cell. In response to this stress, infected cells can induce several defense mechanisms to promote cell survival and limit the use of energy and nutrients, which can culminate in a global reduction of protein synthesis. These mechanisms can target the subcellular localization of mRNAs, the activity of cellular translation factors, or the induction of specific translational reprogramming. Yet, to ensure that viral protein synthesis continues despite the host response or viral modulation of the translation machinery, viruses have evolved diverse strategies to outcompete cellular mRNAs and harness host translation capacity by evolving alternative translation mechanisms.

With recent examples of modulation of key cellular signaling nodes controlling translational activity during infection, novel understanding of viral hijacking of the ribosomal machinery at the structural and biochemical levels, expanding coding capacity by viruses, and increased appreciation of how the cellular landscape of translation is remodeled during infection, Pathogens is launching a Special Issue focused on “Translational Control at the Virus–Host Interface”.

Prof. Nicolas Locker
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 papers will be 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. Pathogens 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 1800 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

  • translation
  • viruses
  • eIFs
  • signaling
  • translatome
  • cap-independent translation

Published Papers (1 paper)

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Research

Open AccessArticle
Candidate Gene Markers Associated with Fecal Shedding of the Feline Enteric Coronavirus (FECV)
Pathogens 2020, 9(11), 958; https://doi.org/10.3390/pathogens9110958 - 17 Nov 2020
Cited by 1 | Viewed by 749
Abstract
The Feline coronavirus (FCoV) can cause a fatal disease, the Feline Infectious Peritonitis. Persistent shedders represent the most important source of infection. The role of the host in FCoV fecal shedding is unknown. The objective of this study was to develop gene markers [...] Read more.
The Feline coronavirus (FCoV) can cause a fatal disease, the Feline Infectious Peritonitis. Persistent shedders represent the most important source of infection. The role of the host in FCoV fecal shedding is unknown. The objective of this study was to develop gene markers and to test their associations with FCoV shedding patterns. Fecal samples were taken from 57 cats of 12 breeds on the day 0 and after 2, 4 and 12 months. Variation from persistent and/or high-intensity shedding to no shedding was observed. Thirteen immunity-related genes were selected as functional and positional/functional candidates. Positional candidates were selected in a candidate region detected by a GWAS analysis. Tens to hundreds of single nucleotide polymorphisms (SNPs) per gene were identified using next generation sequencing. Associations with different phenotypes were assessed by chi-square and Fisher’s exact tests. SNPs of one functional and one positional candidate (NCR1 and SLX4IP, respectively) and haplotypes of four genes (SNX5, NCR2, SLX4IP, NCR1) were associated with FCoV shedding at pcorected < 0.01. Highly significant associations were observed for extreme phenotypes (persistent/high-intensity shedders and non-shedders) suggesting that there are two major phenotypes associated with different genotypes, highly susceptible cats permanently shedding high amounts of viral particles and resistant non-shedders. Full article
(This article belongs to the Special Issue Translational Control at the Virus–Host Interface)
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