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Special Issue "Viral Infections of the CNS"

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

Deadline for manuscript submissions: closed (31 March 2014)

Special Issue Editors

Guest Editor
Prof. Dr. Michel Brahic (Website)

Department of Microbiology Immunology, Stanford University School of Medicine, Fairchild Building, 299 Campus Drive, Stanford, CA 94305, USA
Phone: +650 498 7085
Fax: +650 498 7147
Guest Editor
Dr. Daniel Gonzalez-Dunia (Website)

Team 9: Pathogenesis of viral infections of the central nervous system, Centre de Physiopathologie de Toulouse-Purpan, Inserm UMR1043 - CNRS UMR5282 - Université Toulouse III, CHU Purpan - BP 3028, 31024 Toulouse Cedex 3, France
Phone: +33 5 6274 4511
Fax: +33 5 6274 4558

Special Issue Information

Submission

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. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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 refereed through a 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 1500 CHF (Swiss Francs).

Keywords

  • neurotropism
  • neuroinvasion
  • axonal transport
  • pathogenesis
  • demyelination
  • neuronal activity
  • immune responses in the CNS
  • neuron
  • astrocyte
  • oligodendrocyte
  • microglia
  • synapse
  • trans-synaptic
  • synaptic plasticity
  • brain/blood barrier
  • choroid plexus
  • encephalitis
  • myelitis
  • encephalomyelitis
  • dementia

Published Papers (3 papers)

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Review

Open AccessReview Antiviral Type I and Type III Interferon Responses in the Central Nervous System
Viruses 2013, 5(3), 834-857; doi:10.3390/v5030834
Received: 4 February 2013 / Revised: 11 March 2013 / Accepted: 12 March 2013 / Published: 15 March 2013
Cited by 16 | PDF Full-text (1001 KB) | HTML Full-text | XML Full-text
Abstract
The central nervous system (CNS) harbors highly differentiated cells, such as neurons that are essential to coordinate the functions of complex organisms. This organ is partly protected by the blood-brain barrier (BBB) from toxic substances and pathogens carried in the bloodstream. Yet, [...] Read more.
The central nervous system (CNS) harbors highly differentiated cells, such as neurons that are essential to coordinate the functions of complex organisms. This organ is partly protected by the blood-brain barrier (BBB) from toxic substances and pathogens carried in the bloodstream. Yet, neurotropic viruses can reach the CNS either by crossing the BBB after viremia, or by exploiting motile infected cells as Trojan horses, or by using axonal transport. Type I and type III interferons (IFNs) are cytokines that are critical to control early steps of viral infections. Deficiencies in the IFN pathway have been associated with fatal viral encephalitis both in humans and mice. Therefore, the IFN system provides an essential protection of the CNS against viral infections. Yet, basal activity of the IFN system appears to be low within the CNS, likely owing to the toxicity of IFN to this organ. Moreover, after viral infection, neurons and oligodendrocytes were reported to be relatively poor IFN producers and appear to keep some susceptibility to neurotropic viruses, even in the presence of IFN. This review addresses some trends and recent developments concerning the role of type I and type III IFNs in: i) preventing neuroinvasion and infection of CNS cells; ii) the identity of IFN-producing cells in the CNS; iii) the antiviral activity of ISGs; and iv) the activity of viral proteins of neurotropic viruses that target the IFN pathway. Full article
(This article belongs to the Special Issue Viral Infections of the CNS)
Open AccessReview Directional Spread of Alphaherpesviruses in the Nervous System
Viruses 2013, 5(2), 678-707; doi:10.3390/v5020678
Received: 3 January 2013 / Revised: 4 February 2013 / Accepted: 5 February 2013 / Published: 11 February 2013
Cited by 18 | PDF Full-text (755 KB) | HTML Full-text | XML Full-text
Abstract
Alphaherpesviruses are pathogens that invade the nervous systems of their mammalian hosts. Directional spread of infection in the nervous system is a key component of the viral lifecycle and is critical for the onset of alphaherpesvirus-related diseases. Many alphaherpesvirus infections originate at [...] Read more.
Alphaherpesviruses are pathogens that invade the nervous systems of their mammalian hosts. Directional spread of infection in the nervous system is a key component of the viral lifecycle and is critical for the onset of alphaherpesvirus-related diseases. Many alphaherpesvirus infections originate at peripheral sites, such as epithelial tissues, and then enter neurons of the peripheral nervous system (PNS), where lifelong latency is established. Following reactivation from latency and assembly of new viral particles, the infection typically spreads back out towards the periphery. These spread events result in the characteristic lesions (cold sores) commonly associated with herpes simplex virus (HSV) and herpes zoster (shingles) associated with varicella zoster virus (VZV). Occasionally, the infection spreads transsynaptically from the PNS into higher order neurons of the central nervous system (CNS). Spread of infection into the CNS, while rarer in natural hosts, often results in severe consequences, including death. In this review, we discuss the viral and cellular mechanisms that govern directional spread of infection in the nervous system. We focus on the molecular events that mediate long distance directional transport of viral particles in neurons during entry and egress. Full article
(This article belongs to the Special Issue Viral Infections of the CNS)
Open AccessReview Immune Responses to West Nile Virus Infection in the Central Nervous System
Viruses 2012, 4(12), 3812-3830; doi:10.3390/v4123812
Received: 20 November 2012 / Revised: 7 December 2012 / Accepted: 10 December 2012 / Published: 17 December 2012
Cited by 20 | PDF Full-text (532 KB) | HTML Full-text | XML Full-text
Abstract
West Nile virus (WNV) continues to cause outbreaks of severe neuroinvasive disease in humans and other vertebrate animals in the United States, Europe, and other regions of the world. This review discusses our understanding of the interactions between virus and host that [...] Read more.
West Nile virus (WNV) continues to cause outbreaks of severe neuroinvasive disease in humans and other vertebrate animals in the United States, Europe, and other regions of the world. This review discusses our understanding of the interactions between virus and host that occur in the central nervous system (CNS), the outcome of which can be protection, viral pathogenesis, or immunopathogenesis. We will focus on defining the current state of knowledge of WNV entry, tropism, and host immune response in the CNS, all of which affect the balance between injury and successful clearance. Full article
(This article belongs to the Special Issue Viral Infections of the CNS)

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