Neuropathogenesis of Arboviruses

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

Deadline for manuscript submissions: 15 December 2024 | Viewed by 4458

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Guest Editor
Department of Microbiology & Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA
Interests: emerging and re-emerging RNA viruses; host immunity; neuropathogenesis; vaccine development; antiviral agents
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Special Issue Information

Dear Colleagues,

Arboviruses (arthropod-borne viruses), which are transmitted through the bite of blood-feeding arthropods like mosquitoes, ticks, and sandflies, can trigger neurological disorders. These include encephalitis, paralysis, ophthalmological impairments, developmental defects, or neurological sequelae. Neurological disease caused by arboviral infections often affects young, elderly, and immunocompromised individuals and is becoming a growing public health issue globally. However, the neuropathogenesis of arboviruses is still largely unknown. 

The Special Issue aims to present the latest research on all aspects of the neuropathogenesis of arboviruses. Developing a better understanding of virus–host interactions in the nervous system will be crucial for the development of new therapeutics. Manuscripts of all types are welcome, including reviews, research articles, and short communications. We look forward to your valuable contributions.

Prof. Dr. Tian Wang
Guest Editor

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Keywords

  • vector-borne viruses
  • encephalitis
  • arboviruses
  • neuropathogenesis
  • neuroinvasive
  • neurovirulence
  • blood–brain barrier
  • neuroinflammation
  • flavivirus
  • alphavirus

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Published Papers (2 papers)

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Research

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15 pages, 1959 KiB  
Article
VEEV TC-83 Triggers Dysregulation of the Tryptophan–Kynurenine Pathway in the Central Nervous System That Correlates with Cognitive Impairment in Tg2576 Mice
by Chanida Fongsaran, Kelly T. Dineley, Slobodan Paessler and Irma E. Cisneros
Pathogens 2024, 13(5), 397; https://doi.org/10.3390/pathogens13050397 - 9 May 2024
Viewed by 1448
Abstract
Neurodegenerative diseases are chronic conditions affecting the central nervous system (CNS). Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the accumulation of amyloid beta in the limbic and cortical brain regions. AD is presumed to result from genetic abnormalities or environmental factors, [...] Read more.
Neurodegenerative diseases are chronic conditions affecting the central nervous system (CNS). Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by the accumulation of amyloid beta in the limbic and cortical brain regions. AD is presumed to result from genetic abnormalities or environmental factors, including viral infections, which may have deleterious, long-term effects. In this study, we demonstrate that the Venezuelan equine encephalitis virus (VEEV) commonly induces neurodegeneration and long-term neurological or cognitive sequelae. Notably, the effects of VEEV infection can persistently influence gene expression in the mouse brain, suggesting a potential link between the observed neurodegenerative outcomes and long-term alterations in gene expression. Additionally, we show that alphavirus encephalitis exacerbates the neuropathological profile of AD through crosstalk between inflammatory and kynurenine pathways, generating a range of metabolites with potent effects. Using a mouse model for β-amyloidosis, Tg2576 mice, we found that cognitive deficits and brain pathology were more severe in Tg2576 mice infected with VEEV TC-83 compared to mock-infected controls. Thus, during immune activation, the kynurenine pathway plays a more active role in the VEEV TC-83-infected cells, leading to increases in the abundance of transcripts related to the kynurenine pathway of tryptophan metabolism. This pathway generates several metabolites with potent effects on neurotransmitter systems as well as on inflammation, as observed in VEEV TC-83-infected animals. Full article
(This article belongs to the Special Issue Neuropathogenesis of Arboviruses)
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Review

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24 pages, 3727 KiB  
Review
Zika Virus Neuropathogenesis—Research and Understanding
by Anna D. Metzler and Hengli Tang
Pathogens 2024, 13(7), 555; https://doi.org/10.3390/pathogens13070555 - 2 Jul 2024
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Abstract
Zika virus (ZIKV), a mosquito-borne flavivirus, is prominently associated with microcephaly in babies born to infected mothers as well as Guillain-Barré Syndrome in adults. Each cell type infected by ZIKV—neuronal cells (radial glial cells, neuronal progenitor cells, astrocytes, microglia cells, and glioblastoma stem [...] Read more.
Zika virus (ZIKV), a mosquito-borne flavivirus, is prominently associated with microcephaly in babies born to infected mothers as well as Guillain-Barré Syndrome in adults. Each cell type infected by ZIKV—neuronal cells (radial glial cells, neuronal progenitor cells, astrocytes, microglia cells, and glioblastoma stem cells) and non-neuronal cells (primary fibroblasts, epidermal keratinocytes, dendritic cells, monocytes, macrophages, and Sertoli cells)—displays its own characteristic changes to their cell physiology and has various impacts on disease. Here, we provide an in-depth review of the ZIKV life cycle and its cellular targets, and discuss the current knowledge of how infections cause neuropathologies, as well as what approaches researchers are currently taking to further advance such knowledge. A key aspect of ZIKV neuropathogenesis is virus-induced neuronal apoptosis via numerous mechanisms including cell cycle dysregulation, mitochondrial fragmentation, ER stress, and the unfolded protein response. These, in turn, result in the activation of p53-mediated intrinsic cell death pathways. A full spectrum of infection models including stem cells and co-cultures, transwells to simulate blood–tissue barriers, brain-region-specific organoids, and animal models have been developed for ZIKV research. Full article
(This article belongs to the Special Issue Neuropathogenesis of Arboviruses)
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