Coronavirus neurovirulence correlates with the ability of the virus to induce proinflammatory cytokine signals from astrocytes and microglia. Academic Article uri icon

Overview

abstract

  • The molecular and cellular basis of coronavirus neurovirulence is poorly understood. Since neurovirulence may be determined at the early stages of infection of the central nervous system (CNS), we hypothesize that it may depend on the ability of the virus to induce proinflammatory signals from brain cells for the recruitment of blood-derived inflammatory cells. To test this hypothesis, we studied the interaction between coronaviruses (mouse hepatitis virus) of different neurovirulences with primary cell cultures of brain immune cells (astrocytes and microglia) and mouse tissues. We found that the level of neurovirulence of the virus correlates with its differential ability to induce proinflammatory cytokines (interleukin 12 [IL-12] p40, tumor necrosis factor alpha, IL-6, IL-15, and IL-1beta) in astrocytes and microglia and in mouse brains and spinal cords. These findings suggest that coronavirus neurovirulence may depend on a novel discriminatory ability of astrocytes and microglia to induce a proinflammatory response in the CNS.

publication date

  • April 1, 2004

Research

keywords

  • Astrocytes
  • Coronavirus
  • Cytokines
  • Inflammation Mediators
  • Microglia

Identity

PubMed Central ID

  • PMC371061

Scopus Document Identifier

  • 1842614388

Digital Object Identifier (DOI)

  • 10.1128/jvi.78.7.3398-3406.2004

PubMed ID

  • 15016862

Additional Document Info

volume

  • 78

issue

  • 7