Special Issue "Viruses Ten-Year Anniversary"

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

Deadline for manuscript submissions: 1 December 2019.

Special Issue Editor

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

Special Issue Information

Dear Colleagues,

Viruses was launched by MDPI in 2009. At that time, open access journals were a relatively novel phenomenon, and much of my time as Editor-in-Chief was initially spent explaining the concept of open access and why it is a viable publication model. During the ensuing decade, open access has clearly caught on. There are now innumerable open-access journals, and while many are of dubious quality, funding agencies around the world are increasingly requiring that the research they support be published in an open-access format (1, 2). In 2009, Viruses published only 70 papers; this number swelled to 391 in 2017. The journal’s impact factor, which was 1.5 in 2011, increased to 3.761 in 2017. I am particularly proud of the journal’s outreach activities: we sponsor annual travel awards for students and postdocs and a biennial Viruses Young Investigator Award (3). In 2016 and again in 2018, we organized international virology conferences, held in Basel, Switzerland and Barcelona, Spain, respectively, and we are currently planning the Viruses 2020 conference, to be held again in Barcelona. We now have in place affiliation agreements with five virology societies from three continents: the American Society for Virology (ASV), Spanish Society for Virology (SEV), Canadian Society for Virology (CSV), Italian Society for Virology (SIV-ISV) and Australasian Virology Society (AVS). These agreements benefit the membership of the societies while at the same time increasing the profile of Viruses and promoting virology research globally. The progress that Viruses has made since 2009 would not have been possible without the dedication of the editorial staff and a stellar group of Associate Editors and Editorial Board members.

The past decade has also witnessed enormous developments in the field of virology. A curative therapy for hepatitis C virus (HCV) has been developed (4), and vaccines for human papillomavirus (HPV) are now widely available (5). Progress in a range of technologies, from high-throughput deep sequencing to cryo-electron microscopy, have made possible transformative insights into virus replication at the molecular, cellular, structural, and population levels. Despite this progress, events over the past decade—including global outbreaks of Ebola virus, Zika virus and the MERS coronavirus—have served as constant reminders that viruses will continue to pose a significant threat to human health.

This 10-year anniversary issue brings together a number of leading authors across plant, insect, and animal virology and prion research to share their research and insights. This Special Issue celebrates both the first decade of Viruses and the progress made in the field of virology over the past decade.

References

  1. https://www.ukri.org/funding/information-for-award-holders/open-access/
  2. http://ec.europa.eu/programmes/horizon2020/en/h2020-section/open-science-open-access
  3. https://www.mdpi.com/journal/viruses/awards
  4. http://www.who.int/hepatitis/news-events/hep-c-scale-up/en/
  5. http://www.who.int/immunization/diseases/hpv/en/

Dr. Eric O. Freed
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. 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 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.

Published Papers (9 papers)

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Review

Open AccessReview
Diverse Mechanisms Underlie Enhancement of Enteric Viruses by the Mammalian Intestinal Microbiota
Viruses 2019, 11(8), 760; https://doi.org/10.3390/v11080760 - 17 Aug 2019
Abstract
Over the past two decades, there has been tremendous progress in understanding the impact of the intestinal microbiota on mammalian metabolism, physiology, and immune development and function. There has also been substantial advancement in elucidating the interplay between commensal and pathogenic bacteria. Relatively [...] Read more.
Over the past two decades, there has been tremendous progress in understanding the impact of the intestinal microbiota on mammalian metabolism, physiology, and immune development and function. There has also been substantial advancement in elucidating the interplay between commensal and pathogenic bacteria. Relatively more recently, researchers have begun to investigate the effect of the intestinal microbiota on viral pathogenesis. Indeed, a growing body of literature has reported that commensal bacteria within the mammalian intestinal tract enhance enteric virus infections through a variety of mechanisms. Commensal bacteria or bacterial glycans can increase the stability of enteric viruses, enhance virus binding to host receptors, modulate host immune responses in a proviral manner, expand the numbers of host cell targets, and facilitate viral recombination. In this review, we will summarize the current literature exploring these effects of the intestinal microbiota on enteric virus infections. Full article
(This article belongs to the Special Issue Viruses Ten-Year Anniversary)
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Open AccessReview
Trans-Acting RNA–RNA Interactions in Segmented RNA Viruses
Viruses 2019, 11(8), 751; https://doi.org/10.3390/v11080751 - 14 Aug 2019
Abstract
RNA viruses represent a large and important group of pathogens that infect a broad range of hosts. Segmented RNA viruses are a subclass of this group that encode their genomes in two or more molecules and package all of their RNA segments in [...] Read more.
RNA viruses represent a large and important group of pathogens that infect a broad range of hosts. Segmented RNA viruses are a subclass of this group that encode their genomes in two or more molecules and package all of their RNA segments in a single virus particle. These divided genomes come in different forms, including double-stranded RNA, coding-sense single-stranded RNA, and noncoding single-stranded RNA. Genera that possess these genome types include, respectively, Orbivirus (e.g., Bluetongue virus), Dianthovirus (e.g., Red clover necrotic mosaic virus) and Alphainfluenzavirus (e.g., Influenza A virus). Despite their distinct genomic features and diverse host ranges (i.e., animals, plants, and humans, respectively) each of these viruses uses trans-acting RNA–RNA interactions (tRRIs) to facilitate co-packaging of their segmented genome. The tRRIs occur between different viral genome segments and direct the selective packaging of a complete genome complement. Here we explore the current state of understanding of tRRI-mediated co-packaging in the abovementioned viruses and examine other known and potential functions for this class of RNA–RNA interaction. Full article
(This article belongs to the Special Issue Viruses Ten-Year Anniversary)
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Open AccessReview
Enteroviruses: A Gut-Wrenching Game of Entry, Detection, and Evasion
Viruses 2019, 11(5), 460; https://doi.org/10.3390/v11050460 - 21 May 2019
Abstract
Enteroviruses are a major source of human disease, particularly in neonates and young children where infections can range from acute, self-limited febrile illness to meningitis, endocarditis, hepatitis, and acute flaccid myelitis. The enterovirus genus includes poliovirus, coxsackieviruses, echoviruses, enterovirus 71, and enterovirus D68. [...] Read more.
Enteroviruses are a major source of human disease, particularly in neonates and young children where infections can range from acute, self-limited febrile illness to meningitis, endocarditis, hepatitis, and acute flaccid myelitis. The enterovirus genus includes poliovirus, coxsackieviruses, echoviruses, enterovirus 71, and enterovirus D68. Enteroviruses primarily infect by the fecal–oral route and target the gastrointestinal epithelium early during their life cycles. In addition, spread via the respiratory tract is possible and some enteroviruses such as enterovirus D68 are preferentially spread via this route. Once internalized, enteroviruses are detected by intracellular proteins that recognize common viral features and trigger antiviral innate immune signaling. However, co-evolution of enteroviruses with humans has allowed them to develop strategies to evade detection or disrupt signaling. In this review, we will discuss how enteroviruses infect the gastrointestinal tract, the mechanisms by which cells detect enterovirus infections, and the strategies enteroviruses use to escape this detection. Full article
(This article belongs to the Special Issue Viruses Ten-Year Anniversary)
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Open AccessReview
Manipulation of Epithelial Differentiation by HPV Oncoproteins
Viruses 2019, 11(4), 369; https://doi.org/10.3390/v11040369 - 22 Apr 2019
Abstract
Papillomaviruses replicate and cause disease in stratified squamous epithelia. Epithelial differentiation is essential for the progression of papillomavirus replication, but differentiation is also impaired by papillomavirus-encoded proteins. The papillomavirus E6 and E7 oncoproteins partially inhibit and/or delay epithelial differentiation and some of the [...] Read more.
Papillomaviruses replicate and cause disease in stratified squamous epithelia. Epithelial differentiation is essential for the progression of papillomavirus replication, but differentiation is also impaired by papillomavirus-encoded proteins. The papillomavirus E6 and E7 oncoproteins partially inhibit and/or delay epithelial differentiation and some of the mechanisms by which they do so are beginning to be defined. This review will outline the key features of the relationship between HPV infection and differentiation and will summarize the data indicating that papillomaviruses alter epithelial differentiation. It will describe what is known so far and will highlight open questions about the differentiation-inhibitory mechanisms employed by the papillomaviruses. Full article
(This article belongs to the Special Issue Viruses Ten-Year Anniversary)
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Open AccessReview
Discovery and Further Studies on Giant Viruses at the IHU Mediterranee Infection That Modified the Perception of the Virosphere
Viruses 2019, 11(4), 312; https://doi.org/10.3390/v11040312 - 30 Mar 2019
Cited by 2
Abstract
The history of giant viruses began in 2003 with the identification of Acanthamoeba polyphaga mimivirus. Since then, giant viruses of amoeba enlightened an unknown part of the viral world, and every discovery and characterization of a new giant virus modifies our perception of [...] Read more.
The history of giant viruses began in 2003 with the identification of Acanthamoeba polyphaga mimivirus. Since then, giant viruses of amoeba enlightened an unknown part of the viral world, and every discovery and characterization of a new giant virus modifies our perception of the virosphere. This notably includes their exceptional virion sizes from 200 nm to 2 µm and their genomic complexity with length, number of genes, and functions such as translational components never seen before. Even more surprising, Mimivirus possesses a unique mobilome composed of virophages, transpovirons, and a defense system against virophages named Mimivirus virophage resistance element (MIMIVIRE). From the discovery and isolation of new giant viruses to their possible roles in humans, this review shows the active contribution of the University Hospital Institute (IHU) Mediterranee Infection to the growing knowledge of the giant viruses’ field. Full article
(This article belongs to the Special Issue Viruses Ten-Year Anniversary)
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Open AccessReview
HIV-1 Envelope Glycoprotein at the Interface of Host Restriction and Virus Evasion
Viruses 2019, 11(4), 311; https://doi.org/10.3390/v11040311 - 30 Mar 2019
Cited by 1
Abstract
Without viral envelope proteins, viruses cannot enter cells to start infection. As the major viral proteins present on the surface of virions, viral envelope proteins are a prominent target of the host immune system in preventing and ultimately eliminating viral infection. In addition [...] Read more.
Without viral envelope proteins, viruses cannot enter cells to start infection. As the major viral proteins present on the surface of virions, viral envelope proteins are a prominent target of the host immune system in preventing and ultimately eliminating viral infection. In addition to the well-appreciated adaptive immunity that produces envelope protein-specific antibodies and T cell responses, recent studies have begun to unveil a rich layer of host innate immune mechanisms restricting viral entry. This review focuses on the exciting progress that has been made in this new direction of research, by discussing various known examples of host restriction of viral entry, and diverse viral countering strategies, in particular, the emerging role of viral envelope proteins in evading host innate immune suppression. We will also highlight the effective cooperation between innate and adaptive immunity to achieve the synergistic control of viral infection by targeting viral envelope protein and checking viral escape. Given that many of the related findings were made with HIV-1, we will use HIV-1 as the model virus to illustrate the basic principles and molecular mechanisms on host restriction targeting HIV-1 envelope protein. Full article
(This article belongs to the Special Issue Viruses Ten-Year Anniversary)
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Open AccessReview
IFN Signaling in Inflammation and Viral Infections: New Insights from Fish Models
Viruses 2019, 11(3), 302; https://doi.org/10.3390/v11030302 - 26 Mar 2019
Cited by 1
Abstract
The overarching structure of the type I interferon (IFN) system is conserved across vertebrates. However, the variable numbers of whole genome duplication events during fish evolution offer opportunities for the expansion, diversification, and new functionalization of the genes that are involved in antiviral [...] Read more.
The overarching structure of the type I interferon (IFN) system is conserved across vertebrates. However, the variable numbers of whole genome duplication events during fish evolution offer opportunities for the expansion, diversification, and new functionalization of the genes that are involved in antiviral immunity. In this review, we examine how fish models provide new insights about the implication of virus-driven inflammation in immunity and hematopoiesis. Mechanisms that have been discovered in fish, such as the strong adjuvant effect of type I IFN that is used with DNA vaccination, constitute good models to understand how virus-induced inflammatory mechanisms can interfere with adaptive responses. We also comment on new discoveries regarding the role of pathogen-induced inflammation in the development and guidance of hematopoietic stem cells in zebrafish. These findings raise issues about the potential interferences of viral infections with the establishment of the immune system. Finally, the recent development of genome editing provides new opportunities to dissect the roles of the key players involved in the antiviral response in fish, hence enhancing the power of comparative approaches. Full article
(This article belongs to the Special Issue Viruses Ten-Year Anniversary)
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Open AccessReview
Function, Architecture, and Biogenesis of Reovirus Replication Neoorganelles
Viruses 2019, 11(3), 288; https://doi.org/10.3390/v11030288 - 21 Mar 2019
Cited by 1
Abstract
Most viruses that replicate in the cytoplasm of host cells form neoorganelles that serve as sites of viral genome replication and particle assembly. These highly specialized structures concentrate viral proteins and nucleic acids, prevent the activation of cell-intrinsic defenses, and coordinate the release [...] Read more.
Most viruses that replicate in the cytoplasm of host cells form neoorganelles that serve as sites of viral genome replication and particle assembly. These highly specialized structures concentrate viral proteins and nucleic acids, prevent the activation of cell-intrinsic defenses, and coordinate the release of progeny particles. Reoviruses are common pathogens of mammals that have been linked to celiac disease and show promise for oncolytic applications. These viruses form nonenveloped, double-shelled virions that contain ten segments of double-stranded RNA. Replication organelles in reovirus-infected cells are nucleated by viral nonstructural proteins µNS and σNS. Both proteins partition the endoplasmic reticulum to form the matrix of these structures. The resultant membranous webs likely serve to anchor viral RNA–protein complexes for the replication of the reovirus genome and the assembly of progeny virions. Ongoing studies of reovirus replication organelles will advance our knowledge about the strategies used by viruses to commandeer host biosynthetic pathways and may expose new targets for therapeutic intervention against diverse families of pathogenic viruses. Full article
(This article belongs to the Special Issue Viruses Ten-Year Anniversary)
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Open AccessReview
Packaging of Genomic RNA in Positive-Sense Single-Stranded RNA Viruses: A Complex Story
Viruses 2019, 11(3), 253; https://doi.org/10.3390/v11030253 - 13 Mar 2019
Abstract
The packaging of genomic RNA in positive-sense single-stranded RNA viruses is a key part of the viral infectious cycle, yet this step is not fully understood. Unlike double-stranded DNA and RNA viruses, this process is coupled with nucleocapsid assembly. The specificity of RNA [...] Read more.
The packaging of genomic RNA in positive-sense single-stranded RNA viruses is a key part of the viral infectious cycle, yet this step is not fully understood. Unlike double-stranded DNA and RNA viruses, this process is coupled with nucleocapsid assembly. The specificity of RNA packaging depends on multiple factors: (i) one or more packaging signals, (ii) RNA replication, (iii) translation, (iv) viral factories, and (v) the physical properties of the RNA. The relative contribution of each of these factors to packaging specificity is different for every virus. In vitro and in vivo data show that there are different packaging mechanisms that control selective packaging of the genomic RNA during nucleocapsid assembly. The goals of this article are to explain some of the key experiments that support the contribution of these factors to packaging selectivity and to draw a general scenario that could help us move towards a better understanding of this step of the viral infectious cycle. Full article
(This article belongs to the Special Issue Viruses Ten-Year Anniversary)
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