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Special Issue "Molecular Research on Arboviruses Infection"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 April 2020.

Special Issue Editor

Dr. Byron Martina
E-Mail Website
Guest Editor
Artemis One Health, Delft, Netherlands
Tel. +31 10 7044279
Interests: dengue virus infection

Special Issue Information

Dear Colleagues,

Emerging and existing arboviruses represent a constant threat in all regions of the world. Understanding the molecular mechanisms of pathogenesis and protective immunity is an important endeavour for designing new therapeutic interventions. The molecular pathogenesis of arbovirus infections describes our current understanding of the pathogenesis of selected arboviruses, such as dengue, Zika, West Nile, Rift Valley fever, chikungunya, and many others. Molecular pathogenesis may focus on, but is not restricted to, for instance tropism, host–pathogen interactions at a cellular and molecular level, study of virulence factors, mico-evolution, host resistance to pathogens, and factors driving the emergence of new viruses. Deciphering the specific aberrant cell signalling pathways in disease caused by arboviruses is an important piece in the molecular biology puzzle underlying these diseases. Understanding the ubiquitous pathways implicated in the disease, providing numerous potential therapeutic targets, may also be crucial for researchers in order to move forward. Consider, for instance, dengue, which consists of four serotypes. Although primary infection confers durable, if not life-long protection against re-infection by a homologous dengue virus serotype, secondary infection by a heterologous serotype is considered the most important risk factor for severe disease. However, the molecular mechanisms of, for instance, antibody-dependent enhancement, antibody glycosylation, original antigenic sin, mitochondrial dysfunction, pyroptosis, endothelium cell permeability, and so on, which have been associated with severe diseases remaining poorly understood. This Special Issue aims to bring this knowledge together and to identify the gaps in our understanding of the molecular mechanisms of evolution and pathogenesis.

Dr. Byron Martina
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Arboviruses Infection
  • Virulence Factors
  • Mico-Evolution
  • Molecular Pathogenesis
  • Cell Death
  • Aberrant Cell Signaling Pathways
  • Therapeutic Targets

Published Papers (1 paper)

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Research

Open AccessArticle
Elevation of Cleaved p18 Bax Levels Associated with the Kinetics of Neuronal Cell Death during Japanese Encephalitis Virus Infection
Int. J. Mol. Sci. 2019, 20(20), 5016; https://doi.org/10.3390/ijms20205016 - 10 Oct 2019
Abstract
Japanese encephalitis virus (JEV) infection induces uncontrolled neuronal apoptosis, leading to irreversible brain damage. However, the mechanism of JEV-induced neuronal apoptosis has not been clearly elucidated. This study aimed to investigate both virus replication and neuronal cell apoptosis during JEV infection in human [...] Read more.
Japanese encephalitis virus (JEV) infection induces uncontrolled neuronal apoptosis, leading to irreversible brain damage. However, the mechanism of JEV-induced neuronal apoptosis has not been clearly elucidated. This study aimed to investigate both virus replication and neuronal cell apoptosis during JEV infection in human neuroblastoma SH-SY5Y cells. As a result, the kinetic productions of new viral progeny were time- and dose-dependent. The stimulation of SH-SY5Y cell apoptosis was dependent on the multiplicity of infections (MOIs) and infection periods, particularly during the late period of infection. Interestingly, we observed that of full-length Bax (p21 Bax) level started to decrease, which corresponded to the increased level of its cleaved form (p18 Bax). The formation of p18 Bax resulting in cytochrome c release into the cytosol appeared to correlate with JEV-induced apoptotic cell death together with the activation of caspase-3/7 activity, especially during the late stage of a robust viral infection. Therefore, our results suggest another possible mechanism of JEV-induced apoptotic cell death via the induction of the proteolysis of endogenous p21 Bax to generate p18 Bax. This finding could be a new avenue to facilitate novel drug discovery for the further development of therapeutic treatments that could relieve neuronal damage from JEV infection. Full article
(This article belongs to the Special Issue Molecular Research on Arboviruses Infection)
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