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Special Issue "Viral Entry Pathways"

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

Deadline for manuscript submissions: 31 July 2019

Special Issue Editors

Guest Editor
Prof. Dr. Anthony V. Nicola

Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA
Website | E-Mail
Interests: virology; virus-host interactions; viral entry; antivirals; herpesviruses; endocytosis; membrane fusion; viral glycoproteins
Guest Editor
Prof. Dr. Lijun Rong

Department of Microbiology and Immunology, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA
Website | E-Mail
Phone: 3123550203
Interests: entry mechanisms of several enveloped viruses such as filoviruses and influenza A viruses; the development of antivirals
Guest Editor
Prof. Dr. Lu Lu

Key Laboratory of Medical Molecular Virology of Ministries of Health and Education, School of Basic Medical Sciences Fudan University, Shanghai 200032, China
Website | E-Mail
Interests: mechanisms of viral entry; viral mediated membrane fusion; virus structures; viral entry inhibitor; antiviral vaccine

Special Issue Information

Dear Colleagues,

Viral entry is the first step of infection in the viral life cycle and an important antiviral target. This process is initiated by specific interactions between a virus protein(s) with host factors on the host cells, and followed by diverse pathways such as endocytosis, membrane fusion, and/or viral penetration to enter the target cells. Recent work using an integral approach of cell biology studies, live-cell imaging, structural biology, and systems biology has provided new insights into the multiple and subtly different pathways that viruses use to enter host cells.
In this Special Issue, we welcome submissions of research or review articles on recent advances in our understanding of viral entry pathways. Topics may include but are not limited to the cell and molecular biology of viral entry, virus–host interactions, cellular receptors, viral structures, and antivirals of both DNA and RNA viruses.

Prof. Dr. Anthony V. Nicola
Prof. Dr. Lijun Rong
Prof. Dr. Lu Lu
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 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

  • viral entry pathways
  • endocytic entry
  • viral membrane fusion
  • viral penetration
  • virus-host interactions
  • virus receptor
  • viral entry inhibitor
  • antivirals

Published Papers (2 papers)

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Research

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Open AccessArticle
Screening of an FDA-Approved Drug Library with a Two-Tier System Identifies an Entry Inhibitor of Severe Fever with Thrombocytopenia Syndrome Virus
Viruses 2019, 11(4), 385; https://doi.org/10.3390/v11040385
Received: 16 April 2019 / Revised: 23 April 2019 / Accepted: 24 April 2019 / Published: 25 April 2019
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Abstract
Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging tick-borne bunyavirus that causes severe disease in humans with case-fatality rates of up to 30%. There are currently very limited treatment options for SFTSV infection. We conducted a drug repurposing program by establishing [...] Read more.
Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging tick-borne bunyavirus that causes severe disease in humans with case-fatality rates of up to 30%. There are currently very limited treatment options for SFTSV infection. We conducted a drug repurposing program by establishing a two-tier test system to rapidly screen a Food and Drug Administration- (FDA)-approved drug library for drug compounds with anti-SFTSV activity in vitro. We identified five drug compounds that inhibited SFTSV replication at low micromolar concentrations, including hexachlorophene, triclosan, regorafenib, eltrombopag, and broxyquinoline. Among them, hexachlorophene was the most potent with an IC50 of 1.3 ± 0.3 µM and a selectivity index of 18.7. Mechanistic studies suggested that hexachlorophene was a virus entry inhibitor, which impaired SFTSV entry into host cells by interfering with cell membrane fusion. Molecular docking analysis predicted that the binding of hexachlorophene with the hydrophobic pocket between domain I and domain III of the SFTSV Gc glycoprotein was highly stable. The novel antiviral activity and mechanism of hexachlorophene in this study would facilitate the use of hexachlorophene as a lead compound to develop more entry inhibitors with higher anti-SFTSV potency and lower toxicity. Full article
(This article belongs to the Special Issue Viral Entry Pathways)
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Review

Jump to: Research

Open AccessReview
Competitive Cooperation of Hemagglutinin and Neuraminidase during Influenza A Virus Entry
Viruses 2019, 11(5), 458; https://doi.org/10.3390/v11050458
Received: 30 April 2019 / Revised: 17 May 2019 / Accepted: 18 May 2019 / Published: 20 May 2019
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Abstract
The hemagglutinin (HA) and neuraminidase (NA) of influenza A virus possess antagonistic activities on interaction with sialic acid (SA), which is the receptor for virus attachment. HA binds SA through its receptor-binding sites, while NA is a receptor-destroying enzyme by removing SAs. The [...] Read more.
The hemagglutinin (HA) and neuraminidase (NA) of influenza A virus possess antagonistic activities on interaction with sialic acid (SA), which is the receptor for virus attachment. HA binds SA through its receptor-binding sites, while NA is a receptor-destroying enzyme by removing SAs. The function of HA during virus entry has been extensively investigated, however, examination of NA has long been focused to its role in the exit of progeny virus from infected cells, and the role of NA in the entry process is still under-appreciated. This review summarizes the current understanding of the roles of HA and NA in relation to each other during virus entry. Full article
(This article belongs to the Special Issue Viral Entry Pathways)
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