Special Issue "Viruses 2016 - At the Forefront of Virus-Host Interactions"

A special issue of Viruses (ISSN 1999-4915).

Deadline for manuscript submissions: closed (1 August 2016).

Special Issue Editors

Dr. Eric O. Freed
E-Mail Website
Guest Editor
Director, HIV Dynamics and Replication Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201, USA
Tel. 301-846-6223
Special Issues and Collections in MDPI journals
Prof. Dr. Thomas Klimkait
E-Mail Website
Guest Editor
Department of Biomedicine, University of Basel, Petersplatz 10, CH-4051 Basel, Switzerland
Tel. +41 61 267 3264
Interests: RNA viruses; retroviruses; HIV tropism; viral drug resistance; viral reservoirs and eradication; molecular diagnostics in rural settings; 90-90-90 (UNAIDS); archiving viruses

Special Issue Information

Dear Colleagues,

The last few years have witnessed enormous progress in virology research, with major breakthroughs taking place across a wide range of virology-related disciplines. At the same time, the global impact of viral infections on human health has never been more clear. The conference Viruses 2016 - At the Forefront of Virus-Host Interactions, held in Basel, Switzerland from 26th to 28th of January 2016, brought together leading virologists from around the world to share recent developments in their research. The sessions were organized in a theme-based manner, with related topics discussed from the perspective of diverse viruses, ranging from bacteriophage, plant, and insect viruses to animal viruses.

We are organizing a special issue based on the topics presented and discussed at the Viruses 2016
conference.

Topics will include:

General Topics in Virology
Antiviral Innate Immunity
Non-Coding RNAs
Interactions Between Viruses and Membranes
Replication Organelles

We welcome submissions from all meeting participants.  These can be reviews, research articles, commentaries, etc.

Dr. Eric Freed
Prof. Dr. Thomas Klimkait

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 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. 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 2000 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.

Published Papers (5 papers)

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Research

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Open AccessArticle
Accurate Measurement of the Effects of All Amino-Acid Mutations on Influenza Hemagglutinin
Viruses 2016, 8(6), 155; https://doi.org/10.3390/v8060155 - 03 Jun 2016
Cited by 66
Abstract
Influenza genes evolve mostly via point mutations, and so knowing the effect of every amino-acid mutation provides information about evolutionary paths available to the virus. We and others have combined high-throughput mutagenesis with deep sequencing to estimate the effects of large numbers of [...] Read more.
Influenza genes evolve mostly via point mutations, and so knowing the effect of every amino-acid mutation provides information about evolutionary paths available to the virus. We and others have combined high-throughput mutagenesis with deep sequencing to estimate the effects of large numbers of mutations to influenza genes. However, these measurements have suffered from substantial experimental noise due to a variety of technical problems, the most prominent of which is bottlenecking during the generation of mutant viruses from plasmids. Here we describe advances that ameliorate these problems, enabling us to measure with greatly improved accuracy and reproducibility the effects of all amino-acid mutations to an H1 influenza hemagglutinin on viral replication in cell culture. The largest improvements come from using a helper virus to reduce bottlenecks when generating viruses from plasmids. Our measurements confirm at much higher resolution the results of previous studies suggesting that antigenic sites on the globular head of hemagglutinin are highly tolerant of mutations. We also show that other regions of hemagglutinin—including the stalk epitopes targeted by broadly neutralizing antibodies—have a much lower inherent capacity to tolerate point mutations. The ability to accurately measure the effects of all influenza mutations should enhance efforts to understand and predict viral evolution. Full article
(This article belongs to the Special Issue Viruses 2016 - At the Forefront of Virus-Host Interactions)
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Review

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Open AccessReview
The Peculiar Characteristics of Fish Type I Interferons
Viruses 2016, 8(11), 298; https://doi.org/10.3390/v8110298 - 02 Nov 2016
Cited by 23
Abstract
Antiviral type I interferons (IFNs) have been discovered in fish. Genomic studies revealed their considerable number in many species; some genes encode secreted and non-secreted isoforms. Based on cysteine motifs, fish type I IFNs fall in two subgroups, which use two different receptors. [...] Read more.
Antiviral type I interferons (IFNs) have been discovered in fish. Genomic studies revealed their considerable number in many species; some genes encode secreted and non-secreted isoforms. Based on cysteine motifs, fish type I IFNs fall in two subgroups, which use two different receptors. Mammalian type I IFN genes are intronless while type III have introns; in fish, all have introns, but structurally, both subgroups belong to type I. Type I IFNs likely appeared early in vertebrates as intron containing genes, and evolved in parallel in tetrapods and fishes. The diversity of their repertoires in fish and mammals is likely a convergent feature, selected as a response to the variety of viral strategies. Several alternative nomenclatures have been established for different taxonomic fish groups, calling for a unified system. The specific functions of each type I gene remains poorly understood, as well as their interactions in antiviral responses. However, distinct induction pathways, kinetics of response, and tissue specificity indicate that fish type I likely are highly specialized, especially in groups where they are numerous such as salmonids or cyprinids. Unravelling their functional integration constitutes the next challenge to understand how these cytokines evolved to orchestrate antiviral innate immunity in vertebrates. Full article
(This article belongs to the Special Issue Viruses 2016 - At the Forefront of Virus-Host Interactions)
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Open AccessReview
Ubiquitin in Influenza Virus Entry and Innate Immunity
Viruses 2016, 8(10), 293; https://doi.org/10.3390/v8100293 - 24 Oct 2016
Cited by 23
Abstract
Viruses are obligatory cellular parasites. Their mission is to enter a host cell, to transfer the viral genome, and to replicate progeny whilst diverting cellular immunity. The role of ubiquitin is to regulate fundamental cellular processes such as endocytosis, protein degradation, and immune [...] Read more.
Viruses are obligatory cellular parasites. Their mission is to enter a host cell, to transfer the viral genome, and to replicate progeny whilst diverting cellular immunity. The role of ubiquitin is to regulate fundamental cellular processes such as endocytosis, protein degradation, and immune signaling. Many viruses including influenza A virus (IAV) usurp ubiquitination and ubiquitin-like modifications to establish infection. In this focused review, we discuss how ubiquitin and unanchored ubiquitin regulate IAV host cell entry, and how histone deacetylase 6 (HDAC6), a cytoplasmic deacetylase with ubiquitin-binding activity, mediates IAV capsid uncoating. We also discuss the roles of ubiquitin in innate immunity and its implications in the IAV life cycle. Full article
(This article belongs to the Special Issue Viruses 2016 - At the Forefront of Virus-Host Interactions)
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Open AccessReview
Multi-Omics Studies towards Novel Modulators of Influenza A Virus–Host Interaction
Viruses 2016, 8(10), 269; https://doi.org/10.3390/v8100269 - 29 Sep 2016
Cited by 12
Abstract
Human influenza A viruses (IAVs) cause global pandemics and epidemics. These viruses evolve rapidly, making current treatment options ineffective. To identify novel modulators of IAV–host interactions, we re-analyzed our recent transcriptomics, metabolomics, proteomics, phosphoproteomics, and genomics/virtual ligand screening data. We identified 713 potential [...] Read more.
Human influenza A viruses (IAVs) cause global pandemics and epidemics. These viruses evolve rapidly, making current treatment options ineffective. To identify novel modulators of IAV–host interactions, we re-analyzed our recent transcriptomics, metabolomics, proteomics, phosphoproteomics, and genomics/virtual ligand screening data. We identified 713 potential modulators targeting 199 cellular and two viral proteins. Anti-influenza activity for 48 of them has been reported previously, whereas the antiviral efficacy of the 665 remains unknown. Studying anti-influenza efficacy and immuno/neuro-modulating properties of these compounds and their combinations as well as potential viral and host resistance to them may lead to the discovery of novel modulators of IAV–host interactions, which might be more effective than the currently available anti-influenza therapeutics. Full article
(This article belongs to the Special Issue Viruses 2016 - At the Forefront of Virus-Host Interactions)
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Other

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Open AccessCommentary
Vesicular Nucleo-Cytoplasmic Transport—Herpesviruses as Pioneers in Cell Biology
Viruses 2016, 8(10), 266; https://doi.org/10.3390/v8100266 - 27 Sep 2016
Cited by 6
Abstract
Herpesviruses use a vesicle-mediated transfer of intranuclearly assembled nucleocapsids through the nuclear envelope (NE) for final maturation in the cytoplasm. The molecular basis for this novel vesicular nucleo-cytoplasmic transport is beginning to be elucidated in detail. The heterodimeric viral nuclear egress complex (NEC), [...] Read more.
Herpesviruses use a vesicle-mediated transfer of intranuclearly assembled nucleocapsids through the nuclear envelope (NE) for final maturation in the cytoplasm. The molecular basis for this novel vesicular nucleo-cytoplasmic transport is beginning to be elucidated in detail. The heterodimeric viral nuclear egress complex (NEC), conserved within the classical herpesviruses, mediates vesicle formation from the inner nuclear membrane (INM) by polymerization into a hexagonal lattice followed by fusion of the vesicle membrane with the outer nuclear membrane (ONM). Mechanisms of capsid inclusion as well as vesicle-membrane fusion, however, are largely unclear. Interestingly, a similar transport mechanism through the NE has been demonstrated in nuclear export of large ribonucleoprotein complexes during Drosophila neuromuscular junction formation, indicating a widespread presence of a novel concept of cellular nucleo-cytoplasmic transport. Full article
(This article belongs to the Special Issue Viruses 2016 - At the Forefront of Virus-Host Interactions)
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