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Viruses
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Iridoviruses, 2nd Edition
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Iridoviruses, 2nd Edition

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

Deadline for manuscript submissions: 30 September 2024 | Viewed by 613

Special Issue Editors

Prof. Dr. Jian Zhang

E-Mail Website
Guest Editor
School of Ocean, Yantai University, Yantai 264005, China
Interests: iridovirus; anti-viral immune responses of teleost; innate immunity; host-virus interaction
Special Issues, Collections and Topics in MDPI journals
Dr. Thomas B. Waltzek

E-Mail Website
Guest Editor
Department of Infectious Diseases and Immunology, University of Florida, Gainesville, FL 32611, USA
Interests: viral phylodynamics; epidemiology; diagnostics; taxonomy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Iridoviruses are large, icosahedral viruses with double-stranded DNA genomes ranging in size from 103 to 220 kbp that infect a diverse array of invertebrates and cold-blooded (ectothermic) vertebrates. Currently, the complete genomic sequences of more than 40 iridoviruses are available. The current International Committee on Taxonomy of Viruses (ICTV) report classifies members of the family Iridoviridae into two subfamilies: Alphairidovirinae and Betairidovirinae. The former comprises three genera (Ranavirus, Megalocytivirus, and Lymphocystivirus), which mainly infect ectothermic vertebrates, as does the latter (Iridovirus, Chloriridovirus, and Decapodiridovirus), whose members infect primarily invertebrates. Among these genera, ranaviruses and megalocytiviruses are significant pathogens affecting vertebrates, leading to high levels of mortality in commercially and ecologically important fish and amphibians. Recently emerged Decapodiridoviruses have demonstrated a detrimental impact on crustaceans and have thus received increasing attention. This Special Issue aims to publish all types of manuscripts (i.e., reviews, research articles, and short communications) covering a wide range of topics related to iridoviruses, including, but not limited to: the biology of iridoviruses, the pathogenesis of iridoviruses, virus-host interactions, immune responses to iridoviruses, the identification of new species and/or new iridovirus variants, and iridoviruses-based vaccines.

Prof. Dr. Jian Zhang
Dr. Thomas Waltzek
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 submissions that pass pre-check are 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 2600 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

  • iridovirus
  • viral immune evasion
  • anti-viral immune responses
  • viral vaccine
  • viral pathogenesis
  • viral epidemiology

Related Special Issue

Published Papers (2 papers)

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15 pages, 5804 KiB  
Article
ISKNV Triggers AMPK/mTOR-Mediated Autophagy Signaling through Oxidative Stress, Inducing Antioxidant Enzyme Expression and Enhancing Viral Replication in GF-1 Cells
by Tsai-Ching Hsueh, Pin-Han Chen and Jiann-Ruey Hong
Viruses 2024, 16(6), 914; https://doi.org/10.3390/v16060914 - 4 Jun 2024
Abstract
Infectious spleen and kidney necrosis virus (ISKNV) infections can induce the process of host cellular autophagy but have rarely been identified within the molecular autophagy signaling pathway. In the present study, we demonstrated that ISKNV induces ROS-mediated oxidative stress signals for the induction [...] Read more.
Infectious spleen and kidney necrosis virus (ISKNV) infections can induce the process of host cellular autophagy but have rarely been identified within the molecular autophagy signaling pathway. In the present study, we demonstrated that ISKNV induces ROS-mediated oxidative stress signals for the induction of 5′AMP-activated protein kinase/mechanistic target of rapamycin kinase (AMPK/mTOR)-mediated autophagy and upregulation of host antioxidant enzymes in fish GF-1 cells. We also examined ISKNV-induced oxidative stress, finding that reactive oxidative species (ROS) increased by 1.5-fold and 2.5-fold from day 2 to day 3, respectively, as assessed by the H2DCFDA assay for tracing hydrogen peroxide (H2O2), which was blocked by NAC treatment in fish GF-1 cells. Furthermore, ISKNV infection was shown to trigger oxidative stress/Nrf2 signaling from day 1 to day 3; this event was then correlated with the upregulation of antioxidant enzymes such as Cu/ZnSOD and MnSOD and was blocked by the antioxidant NAC. Using an MDC assay, TEM analysis and autophagy marker LC3-II/I ratio, we found that ROS stress can regulate autophagosome formation within the induction of autophagy, which was inhibited by NAC treatment in GF-1 cells. Through signal analysis, we found that AMPK/mTOR flux was modulated through inhibition of mTOR and activation of AMPK, indicating phosphorylation levels of mTOR Ser 2448 and AMPK Thr 172 from day 1 to day 3; however, this process was reversed by NAC treatment, which also caused a reduction in virus titer (TCID50%) of up to 1000 times by day 3 in GF-1 cells. Thus, ISKNV-induced oxidative stress signaling is blocked by antioxidant NAC, which can also either suppress mTOR/AMPK autophagic signals or reduce viral replication. These findings may provide the basis for the creation of DNA control and treatment strategies. Full article
(This article belongs to the Special Issue Iridoviruses, 2nd Edition)
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13 pages, 4100 KiB  
Brief Report
Cytokinins Reduce Viral Replication and Alter Plaque Morphology of Frog Virus 3 In Vitro
by Mark Seegobin, Samantha R. Logan, R. J. Neil Emery and Craig R. Brunetti
Viruses 2024, 16(6), 826; https://doi.org/10.3390/v16060826 - 23 May 2024
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Abstract
Cytokinins (CKs) are a group of N6-substituted signaling molecules whose biosynthesis and metabolism have been documented in all kingdoms of life, including vertebrates. While their biological relevance in vertebrate systems continues to be elucidated, they have broadly been documented with therapeutic [...] Read more.
Cytokinins (CKs) are a group of N6-substituted signaling molecules whose biosynthesis and metabolism have been documented in all kingdoms of life, including vertebrates. While their biological relevance in vertebrate systems continues to be elucidated, they have broadly been documented with therapeutic effects in exogenous applications. In this study, we evaluated the virostatic potential of four types of CKs including, N6-isopentenyladenine (iP), N6-isopentenyladenosine (iPR), N6-isopentenyladenosine-5′monophosphate (iPMP), and 2-methylthiol-N6-isopentenyladenosine (2MeSiPR) against the ranavirus type species, frog virus 3 (FV3). Following concurrent treatment and infection, iP and iPR reduced viral replication by 33.8% and 59.6%, respectively, in plaque formation assays. A decrease in viral replication was also observed when CK exposure was limited to 12 h prior to infection, where iP and iPR reduced viral replication by 31% and 23.75%, respectively. Treatment with iP and iPR was also marked by 48% and 60% decreases in viral load over 72 h, respectively, as measured in single step growth curves. Plaque morphology was altered in vitro, as iP and iPR treatment increased plaque area by 83% and 112% with lytic zone formation also becoming more prevalent in corresponding treatments. Treatment with iPMP and 2MeSiPR resulted in no effect on viral kinetics in vitro. The results of this study are the first to provide evidence of CK antiviral activity against a DNA virus and highlight the importance of their structure for therapeutic investigations. Full article
(This article belongs to the Special Issue Iridoviruses, 2nd Edition)
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