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Pathogens
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Host–Virus Interactions in the Nervous System
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Host–Virus Interactions in the Nervous System

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Viral Pathogens".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 4863

Special Issue Editor

Dr. Kathlyn Laval

E-Mail Website
Guest Editor
Laboratory of Virology, Department of Translational Physiology, Infectiology and Public Health, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium
Interests: herpesviruses; neuroinflammation; nervous system; mouse model; neurodegeneration

Special Issue Information

Dear Colleagues,

Viral infections of the nervous system are an important cause of human disease. The outcome of a viral infection within the nervous system depends on a complex interaction between the virus, the neuron, and the immune system. In this Special Issue of Pathogens, we invite both original research articles and reviews that provide novel insights into virus–host interactions in the nervous system. Of particular interest will be manuscripts that advance our current understanding of:

  • The mechanisms of virus entry and spread in the PNS and CNS;
  • The innate immune responses to viral infection that promote viral clearance in the nervous system;
  • The viral immune evasive strategies that support viral replication and spread in neurons;
  • Virus–host interactions that can lead to short-term and long-term neurological disease.

We aim to bring together researchers from a diverse range of virus families (e.g., Herpesviridae, Coronaviridae, Flaviviridae, Orthomyxoviridae and Paramyxoviridae) with a common interest in the virus–host interface in the nervous system by presenting both in vitro and in vivo experimental and clinical studies. A better understanding of virus–host interactions in the nervous system is crucial for the development of new therapeutics against neurotropic infections and associated neurodegeneration. As the neurovirology field has been rapidly expanding over the past few years, our efforts in this Special Issue stand to make a real contribution for improving human health. We look forward to your contribution.

Dr. Kathlyn Laval
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 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. Pathogens 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 2700 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

  • neurotropic viruses
  • peripheral and central nervous system
  • virus-host cell interactions
  • viral entry
  • evasion of innate immunity
  • animal models
  • neuroimmune mechanisms
  • neurodegeneration

Published Papers (3 papers)

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Research

18 pages, 12208 KiB  
Communication
Human Adenovirus Entry and Early Events during Infection of Primary Murine Neurons: Immunofluorescence Studies In Vitro
by Anna Słońska, Aleksandra Miedzińska, Marcin Chodkowski, Piotr Bąska, Aleksandra Mielnikow, Michalina Bartak, Marcin W. Bańbura and Joanna Cymerys
Pathogens 2024, 13(2), 158; https://doi.org/10.3390/pathogens13020158 - 9 Feb 2024
Viewed by 938
Abstract
Human adenovirus (HAdV) is a common pathogen, which can lead to various clinical symptoms and—in some cases—central nervous system (CNS) dysfunctions, such as encephalitis and meningitis. Although the initial events of virus entry have already been identified in various cell types, the mechanism [...] Read more.
Human adenovirus (HAdV) is a common pathogen, which can lead to various clinical symptoms and—in some cases—central nervous system (CNS) dysfunctions, such as encephalitis and meningitis. Although the initial events of virus entry have already been identified in various cell types, the mechanism of neuronal uptake of adenoviruses is relatively little understood. The aim of this study was to investigate early events during adenoviral infection, in particular to determine the connection between cellular coxsackievirus and adenovirus receptor (CAR), clathrin, caveolin, and early endosomal proteins (EEA1 and Rab5) with the entry of HAdVs into primary murine neurons in vitro. An immunofluorescence assay and confocal microscopy analysis were carried out to determine HAdV4, 5, and 7 correlation with CAR, clathrin, caveolin, and early endosomal proteins in neurons. The quantification of Pearson’s coefficient between CAR and HAdVs indicated that the HAdV4 and HAdV5 types correlated with CAR and that the correlation was more substantial for HAdV5. Inhibition of clathrin-mediated endocytosis using chlorpromazine limited the infection with HAdV, whereas inhibition of caveolin-mediated endocytosis did not affect virus entry. Thus, the entry of tested HAdV types into neurons was most likely associated with clathrin but not caveolin. It was also demonstrated that HAdVs correlate with the Rab proteins (EEA1, Rab5) present in early vesicles, and the observed differences in the manner of correlation depended on the serotype of the virus. With our research, we strove to expand knowledge regarding the mechanism of HAdV entry into neurons, which may be beneficial for developing potential therapeutics in the future. Full article
(This article belongs to the Special Issue Host–Virus Interactions in the Nervous System)
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14 pages, 2418 KiB  
Article
Interferon-λ Activates a Differential Response in Peripheral Neurons That Is Effective against Alpha Herpesvirus Infections
by Stephanie Salazar, Khanh T. Y. Luong, Taulima Nua and Orkide O. Koyuncu
Pathogens 2023, 12(9), 1142; https://doi.org/10.3390/pathogens12091142 - 7 Sep 2023
Cited by 3 | Viewed by 1474
Abstract
Alpha herpesviruses (α-HV) infect host mucosal epithelial cells prior to establishing a life-long latent infection in the peripheral nervous system. The initial spread of viral particles from mucosa to the nervous system and the role of intrinsic immune responses at this barrier is [...] Read more.
Alpha herpesviruses (α-HV) infect host mucosal epithelial cells prior to establishing a life-long latent infection in the peripheral nervous system. The initial spread of viral particles from mucosa to the nervous system and the role of intrinsic immune responses at this barrier is not well understood. Using primary neurons cultured in compartmentalized chambers, prior studies performed on Pseudorabies virus (PRV) have demonstrated that type I and type II interferons (IFNs) induce a local antiviral response in axons via distinct mechanisms leading to a reduction in viral particle transport to the neuronal nucleus. A new class of interferons known as type III IFNs has been shown to play an immediate role against viral infection in mucosal epithelial cells. However, the antiviral effects of type III IFNs within neurons during α-HV infection are largely unknown. In this study, we focused on elucidating the antiviral activity of type III IFN against PRV neuronal infection, and we compared the interferon-stimulated gene (ISGs) induction pattern in neurons to non-neuronal cells. We found that IFN pre-exposure of both primary neurons and fibroblast cells significantly reduces PRV virus yield, albeit by differential STAT activation and ISG induction patterns. Notably, we observed that type III IFNs trigger the expression of a subset of ISGs mainly through STAT1 activation to induce an antiviral state in primary peripheral neurons. Full article
(This article belongs to the Special Issue Host–Virus Interactions in the Nervous System)
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12 pages, 2208 KiB  
Article
Establishing a Herpesvirus Quiescent Infection in Differentiated Human Dorsal Root Ganglion Neuronal Cell Line Mediated by Micro-RNA Overexpression
by Yu-Chih Chen, Hedong Li, Miguel Martin-Caraballo and Shaochung Victor Hsia
Pathogens 2022, 11(7), 803; https://doi.org/10.3390/pathogens11070803 - 16 Jul 2022
Cited by 2 | Viewed by 1795
Abstract
HSV-1 is a neurotropic pathogen associated with severe encephalitis, excruciating orofacial sensation, and other chronic neuropathic complications. After the acute infection, the virus may establish a lifelong latency in the neurons of trigeminal ganglia (TG) and other sensory and autonomic ganglia, including the [...] Read more.
HSV-1 is a neurotropic pathogen associated with severe encephalitis, excruciating orofacial sensation, and other chronic neuropathic complications. After the acute infection, the virus may establish a lifelong latency in the neurons of trigeminal ganglia (TG) and other sensory and autonomic ganglia, including the dorsal root ganglia (DRG), etc. The reactivation occurred periodically by a variety of physical or emotional stressors. We have been developing a human DRG neuronal cell-culture model HD10.6, which mimics the mature neurons for latency and reactivation with robust neuronal physiology. We found that miR124 overexpression without acyclovir (ACV) could maintain the virus in a quiescent infection, with the accumulation of latency-associate transcript (LAT). The immediate-early (IE) gene ICP0, on the other hand, was very low and the latent viruses could be reactivated by trichostatin A (TSA) treatment. Together, these observations suggested a putative role of microRNA in promoting HSV-1 latency in human neurons. Full article
(This article belongs to the Special Issue Host–Virus Interactions in the Nervous System)
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