Next Article in Journal
Clinical Characterization of Host Response to Simian Hemorrhagic Fever Virus Infection in Permissive and Refractory Hosts: A Model for Determining Mechanisms of VHF Pathogenesis
Next Article in Special Issue
Mechanisms of Strain Diversity of Disease-Associated in-Register Parallel β-Sheet Amyloids and Implications About Prion Strains
Previous Article in Journal
An Optimized High-Throughput Neutralization Assay for Hepatitis E Virus (HEV) Involving Detection of Secreted Porf2
Previous Article in Special Issue
Prion Strain-Specific Structure and Pathology: A View from the Perspective of Glycobiology
Article Menu
Issue 1 (January) cover image

Export Article

Open AccessReview
Viruses 2019, 11(1), 65; https://doi.org/10.3390/v11010065

Neuroinflammation, Microglia, and Cell-Association during Prion Disease

Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
*
Author to whom correspondence should be addressed.
Received: 24 December 2018 / Revised: 9 January 2019 / Accepted: 10 January 2019 / Published: 15 January 2019
(This article belongs to the Special Issue Deciphering the Molecular Targets of Prion and Prion-Like Strains)
Full-Text   |   PDF [2679 KB, uploaded 15 January 2019]   |  
  |   Review Reports

Abstract

Prion disorders are transmissible diseases caused by a proteinaceous infectious agent that can infect the lymphatic and nervous systems. The clinical features of prion diseases can vary, but common hallmarks in the central nervous system (CNS) are deposition of abnormally folded protease-resistant prion protein (PrPres or PrPSc), astrogliosis, microgliosis, and neurodegeneration. Numerous proinflammatory effectors expressed by astrocytes and microglia are increased in the brain during prion infection, with many of them potentially damaging to neurons when chronically upregulated. Microglia are important first responders to foreign agents and damaged cells in the CNS, but these immune-like cells also serve many essential functions in the healthy CNS. Our current understanding is that microglia are beneficial during prion infection and critical to host defense against prion disease. Studies indicate that reduction of the microglial population accelerates disease and increases PrPSc burden in the CNS. Thus, microglia are unlikely to be a foci of prion propagation in the brain. In contrast, neurons and astrocytes are known to be involved in prion replication and spread. Moreover, certain astrocytes, such as A1 reactive astrocytes, have proven neurotoxic in other neurodegenerative diseases, and thus might also influence the progression of prion-associated neurodegeneration. View Full-Text
Keywords: microglia; astroglia; neuron; neuroinflammation; cytokine; chemokine; PLX5622; prion; scrapie microglia; astroglia; neuron; neuroinflammation; cytokine; chemokine; PLX5622; prion; scrapie
Figures

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Carroll, J.A.; Chesebro, B. Neuroinflammation, Microglia, and Cell-Association during Prion Disease. Viruses 2019, 11, 65.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Viruses EISSN 1999-4915 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top