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Neuroinfectiology: Molecular and Cellular Mechanisms of Neurotropic Virus Infection 2.0
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Neuroinfectiology: Molecular and Cellular Mechanisms of Neurotropic Virus Infection 2.0

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: closed (1 October 2020) | Viewed by 27897

Special Issue Editor

Prof. Dr. Wolfgang Baumgärtner

E-Mail Website
Guest Editor
Department of Pathology, University of Veterinary Medicine, Bünteweg 17, D-30559 Hannover, Germany
Interests: viral pathogenesis; host range; virus-host cell-tropism and interactions;, virus discovery; models for multiple sclerosis; intervention strategies; neuroinfectiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the second volume of our previous Special Issue, “Neuroinfectiology: Molecular and Cellular Mechanisms of Neurotropic Virus Infection”. In recent years, reported cases of viral pathogens causing infection of the central nervous system (CNS) as emerging and re-emerging diseases have been increasing, particularly noticeable in humans and animals. Some viruses will infect only the CNS, others cause a systemic spread and affection of the nervous systems and are noticed in a small percentage of individuals. Still, a substantial number of possible viral CNS diseases remain etiologically undetermined so far. The burden of infectious CNS diseases is reinforced by the fact that survivors may suffer from life-long neurological and psychiatric complications. A sensu stricto definition of neuroinfectiology would refer to a direct pathogen–host cell effect, resulting in cytolysis and inflammation. However, the cellular functions may remain impaired, despite cell survival, especially in the CNS. Such an impaired organ function may be due to a derailment of immune responses, epitope spreading, and molecular mimicry, even after the elimination of the causing viral pathogen. Similarly, predisposing factors, including concurrent diseases and immune deficiencies, may increase susceptibility to viral infection. Therefore, a broader definition of neuroinfectiology should include predisposing mechanisms, acute host–pathogen interactions, and long-term, delayed disturbances and disabilities.

Mechanisms that govern the neuropathogenesis of viral infections will be highlighted in this Special Issue, entitled “Neuroinfectiology: Molecular and Cellular Mechanisms of Neurotropic Virus Infection 2.0”.

Prof. Dr. Wolfgang Baumgärtner
Guest Editor

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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.

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Keywords

  • neuroinfection
  • acute neuropathogenesis
  • long-term pathogenesis
  • neurotoxicity
  • host–glial cell interactions
  • virus discover
  • host range
  • transmission
  • neuro-immunopathology
  • viral persistence
  • demyelination
  • axonopathy
  • delayed neurological symptoms
  • neurocognitive disorders
  • intervention strategies

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Published Papers (5 papers)

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Research

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19 pages, 3303 KiB  
Article
Parainfluenza Virus 5 Infection in Neurological Disease and Encephalitis of Cattle
by Melanie M. Hierweger, Simea Werder and Torsten Seuberlich
Int. J. Mol. Sci. 2020, 21(2), 498; https://doi.org/10.3390/ijms21020498 - 13 Jan 2020
Cited by 18 | Viewed by 4129
Abstract
The etiology of viral encephalitis in cattle often remains unresolved, posing a potential risk for animal and human health. In metagenomics studies of cattle with bovine non-suppurative encephalitis, parainfluenza virus 5 (PIV5) was identified in three brain samples. Interestingly, in two of these [...] Read more.
The etiology of viral encephalitis in cattle often remains unresolved, posing a potential risk for animal and human health. In metagenomics studies of cattle with bovine non-suppurative encephalitis, parainfluenza virus 5 (PIV5) was identified in three brain samples. Interestingly, in two of these animals, bovine herpesvirus 6 and bovine astrovirus CH13 were additionally found. We investigated the role of PIV5 in bovine non-suppurative encephalitis and further characterized the three cases. With traditional sequencing methods, we completed the three PIV5 genomes, which were compared to one another. However, in comparison to already described PIV5 strains, unique features were revealed, like an 81 nucleotide longer open reading frame encoding the small hydrophobic (SH) protein. With in situ techniques, we demonstrated PIV5 antigen and RNA in one animal and found a broad cell tropism of PIV5 in the brain. Comparative quantitative analyses revealed a high viral load of PIV5 in the in situ positive animal and therefore, we propose that PIV5 was probably the cause of the disease. With this study, we clearly show that PIV5 is capable of naturally infecting different brain cell types in cattle in vivo and therefore it is a probable cause of encephalitis and neurological disease in cattle. Full article
(This article belongs to the Special Issue Neuroinfectiology: Molecular and Cellular Mechanisms of Neurotropic Virus Infection 2.0)
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20 pages, 11302 KiB  
Article
Comparison of Theiler’s Murine Encephalomyelitis Virus Induced Spinal Cord and Peripheral Nerve Lesions Following Intracerebral and Intraspinal Infection
by Wen Jin, Eva Leitzen, Sandra Goebbels, Klaus-Armin Nave, Wolfgang Baumgärtner and Florian Hansmann
Int. J. Mol. Sci. 2019, 20(20), 5134; https://doi.org/10.3390/ijms20205134 - 16 Oct 2019
Cited by 7 | Viewed by 2916
Abstract
Hallmarks of Theiler’s murine encephalomyelitis virus (TMEV)-induced demyelinating disease (TMEV-IDD) include spinal cord (SC) inflammation, demyelination and axonal damage occurring approximately 5–8 weeks after classical intracerebral (i.c.) infection. The aim of this study was to elucidate the consequences of intraspinal (i.s.) TMEV infection [...] Read more.
Hallmarks of Theiler’s murine encephalomyelitis virus (TMEV)-induced demyelinating disease (TMEV-IDD) include spinal cord (SC) inflammation, demyelination and axonal damage occurring approximately 5–8 weeks after classical intracerebral (i.c.) infection. The aim of this study was to elucidate the consequences of intraspinal (i.s.) TMEV infection and a direct comparison of classical i.c. and intraspinal infection. Swiss Jim Lambert (SJL)-mice were i.s. infected with the BeAn strain of TMEV. Clinical investigations including a scoring system and rotarod analysis were performed on a regular basis. Necropsies were performed at 3, 7, 14, 28 and 63 days post infection (dpi) following i.s. and at 4, 7, 14, 28, 56, 98, 147 and 196 dpi following i.c. infection. Serial sections of formalin-fixed, paraffin-embedded SC and peripheral nerves (PN) were investigated using hematoxylin and eosin (HE) and immunohistochemistry. I.s. infected mice developed clinical signs and a deterioration of motor coordination approximately 12 weeks earlier than i.c. infected animals. SC inflammation, demyelination and axonal damage occurred approximately 6 weeks earlier in i.s. infected animals. Interestingly, i.s. infected mice developed PN lesions, characterized by vacuolation, inflammation, demyelination and axonal damage, which was not seen following i.c. infection. The i.s. infection model offers the advantage of a significantly earlier onset of clinical signs, inflammatory and demyelinating SC lesions and additionally enables the investigation of virus-mediated PN lesions. Full article
(This article belongs to the Special Issue Neuroinfectiology: Molecular and Cellular Mechanisms of Neurotropic Virus Infection 2.0)
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21 pages, 11511 KiB  
Article
Impact of Astrocyte Depletion upon Inflammation and Demyelination in a Murine Animal Model of Multiple Sclerosis
by Lisa Allnoch, Wolfgang Baumgärtner and Florian Hansmann
Int. J. Mol. Sci. 2019, 20(16), 3922; https://doi.org/10.3390/ijms20163922 - 12 Aug 2019
Cited by 28 | Viewed by 6679
Abstract
Astrocytes play a key role in demyelinating diseases, like multiple sclerosis (MS), although many of their functions remain unknown. The aim of this study was to investigate the impact of astrocyte depletion upon de- and remyelination, inflammation, axonal damage, and virus distribution in [...] Read more.
Astrocytes play a key role in demyelinating diseases, like multiple sclerosis (MS), although many of their functions remain unknown. The aim of this study was to investigate the impact of astrocyte depletion upon de- and remyelination, inflammation, axonal damage, and virus distribution in Theiler’s murine encephalomyelitis (TME). Groups of two to six glial fibrillary acidic protein (GFAP)-thymidine-kinase transgenic SJL mice and SJL wildtype mice were infected with TME virus (TMEV) or mock (vehicle only). Astrocyte depletion was induced by the intraperitoneal administration of ganciclovir during the early and late phase of TME. The animals were clinically investigated while using a scoring system and a rotarod performance test. Necropsies were performed at 46 and 77 days post infection. Cervical and thoracic spinal cord segments were investigated using hematoxylin and eosin (H&E), luxol fast blue-cresyl violet (LFB), immunohistochemistry targeting Amigo2, aquaporin 4, CD3, CD34, GFAP, ionized calcium-binding adapter molecule 1 (Iba1), myelin basic protein (MBP), non-phosphorylated neurofilaments (np-NF), periaxin, S100A10, TMEV, and immunoelectron microscopy. The astrocyte depleted mice showed a deterioration of clinical signs, a downregulation and disorganization of aquaporin 4 in perivascular astrocytes accompanied by vascular leakage. Furthermore, astrocyte depleted mice showed reduced inflammation and lower numbers of TMEV positive cells in the spinal cord. The present study indicates that astrocyte depletion in virus triggered CNS diseases contributes to a deterioration of clinical signs that are mediated by a dysfunction of perivascular astrocytes. Full article
(This article belongs to the Special Issue Neuroinfectiology: Molecular and Cellular Mechanisms of Neurotropic Virus Infection 2.0)
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Review

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14 pages, 342 KiB  
Review
Neuroimaging Findings in Chronic Hepatitis C Virus Infection: Correlation with Neurocognitive and Neuropsychiatric Manifestations
by Matteo Tagliapietra and Salvatore Monaco
Int. J. Mol. Sci. 2020, 21(7), 2478; https://doi.org/10.3390/ijms21072478 - 2 Apr 2020
Cited by 18 | Viewed by 3702
Abstract
Chronic hepatitis C virus (HCV) infection is commonly associated with neurocognitive dysfunction, altered neuropsychological performance and neuropsychiatric symptoms. Quantifiable neuropsychological changes in sustained attention, working memory, executive function, verbal learning and recall are the hallmark of HCV-associated neurocognitive disorder (HCV-AND). This constellation is [...] Read more.
Chronic hepatitis C virus (HCV) infection is commonly associated with neurocognitive dysfunction, altered neuropsychological performance and neuropsychiatric symptoms. Quantifiable neuropsychological changes in sustained attention, working memory, executive function, verbal learning and recall are the hallmark of HCV-associated neurocognitive disorder (HCV-AND). This constellation is at variance with the neuropsychological complex that is seen in minimal hepatic encephalopathy, which is typified by an array of alterations in psychomotor speed, selective attention and visuo-constructive function. Noncognitive symptoms, including sleep disturbances, depression, anxiety and fatigue, which are less easily quantifiable, are frequently encountered and can dominate the clinical picture and the clinical course of patients with chronic HCV infection. More recently, an increased vulnerability to Parkinson’s disease among HCV-infected patients has also been reported. The degree to which neurocognitive and neuropsychiatric changes are due to HCV replication within brain tissues or HCV-triggered peripheral immune activation remain to be determined. Without absolute evidence that clearly exonerates or indicts HCV, our understanding of the so-called “HCV brain syndrome”, relies primarily on clinical and neuropsychological assessments, although other comorbidities and substance abuse may impact on neurocognitive function, thus confounding an appropriate recognition. In recent years, a number of functional and structural brain imaging studies have been of help in recognizing possible biological markers of HCV-AND, thus providing a rationale for guiding and justifying antiviral therapy in selected cases. Here, we review clinical, neuroradiological, and therapeutic responses to interferon-based and interferon-free regimens in HCV-related cognitive and neuropsychiatric disorder. Full article
(This article belongs to the Special Issue Neuroinfectiology: Molecular and Cellular Mechanisms of Neurotropic Virus Infection 2.0)
30 pages, 1432 KiB  
Review
Beneficial and Detrimental Effects of Regulatory T Cells in Neurotropic Virus Infections
by Malgorzata Ciurkiewicz, Vanessa Herder and Andreas Beineke
Int. J. Mol. Sci. 2020, 21(5), 1705; https://doi.org/10.3390/ijms21051705 - 2 Mar 2020
Cited by 16 | Viewed by 9921
Abstract
Neurotropic viruses infect the central nervous system (CNS) and cause acute or chronic neurologic disabilities. Regulatory T cells (Treg) play a critical role for immune homeostasis, but may inhibit pathogen-specific immunity in infectious disorders. The present review summarizes the current knowledge about Treg [...] Read more.
Neurotropic viruses infect the central nervous system (CNS) and cause acute or chronic neurologic disabilities. Regulatory T cells (Treg) play a critical role for immune homeostasis, but may inhibit pathogen-specific immunity in infectious disorders. The present review summarizes the current knowledge about Treg in human CNS infections and their animal models. Besides dampening pathogen-induced immunopathology, Treg have the ability to facilitate protective responses by supporting effector T cell trafficking to the infection site and the development of resident memory T cells. Moreover, Treg can reduce virus replication by inducing apoptosis of infected macrophages and attenuate neurotoxic astrogliosis and pro-inflammatory microglial responses. By contrast, detrimental effects of Treg are caused by suppression of antiviral immunity, allowing for virus persistence and latency. Opposing disease outcomes following Treg manipulation in different models might be attributed to differences in technique and timing of intervention, infection route, genetic background, and the host’s age. In addition, mouse models of virus-induced demyelination revealed that Treg are able to reduce autoimmunity and immune-mediated CNS damage in a disease phase-dependent manner. Understanding the unique properties of Treg and their complex interplay with effector cells represents a prerequisite for the development of new therapeutic approaches in neurotropic virus infections. Full article
(This article belongs to the Special Issue Neuroinfectiology: Molecular and Cellular Mechanisms of Neurotropic Virus Infection 2.0)
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