Related Experiment Video
Updated: Apr 21, 2026
Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Mouse hepatitis virus infection upregulates genes involved in innate immune responses
Dhriti Chatterjee1, Sankar Addya2, Reas S Khan3
1Department of Biological Sciences, Indian Institute of Science Education and Research-Kolkata (IISER-K), Mohanpur, West Bengal, India.
Abstract:
Neurotropic recombinant strain of Mouse Hepatitis Virus, RSA59, induces meningo-encephalitis, myelitis and demyelination following intracranial inoculation. RSA59 induced neuropathology is partially caused by activation of CNS resident microglia, as demonstrated by changes in cellular morphology and increased expression of a microglia/macrophage specific calcium ion binding factor, Iba1. Affymetrix Microarray analysis for mRNA expression data reveals expression of inflammatory mediators that are known to be released by activated microglia. Microglia-specific cell surface molecules, including CD11b, CD74, CD52 and CD68, are significantly upregulated in contrast to CD4, CD8 and CD19. Protein analysis of spinal cord extracts taken from mice 6 days post-inoculation, the time of peak inflammation, reveals robust expression of IFN-γ, IL-12 and mKC. Data suggest that activated microglia and inflammatory mediators contribute to a local CNS microenvironment that regulates viral replication and IFN-γ production during the acute phase of infection, which in turn can cause phagolysosome maturation and phagocytosis of the myelin sheath, leading to demyelination.
Insights
Mouse Hepatitis Virus strain RSA59 causes brain and spinal cord inflammation and demyelination. Activated microglia and inflammatory mediators contribute to this neuropathology during acute infection.
Area of Science:
- Neuroimmunology
- Virology
- Neuroinflammation
Background:
- Mouse Hepatitis Virus strain RSA59 causes meningo-encephalitis, myelitis, and demyelination.
- Activated microglia play a role in the central nervous system (CNS) pathology induced by RSA59.
Purpose of the Study:
- To investigate the role of microglia activation and inflammatory mediators in RSA59-induced neuropathology.
- To understand the molecular mechanisms underlying demyelination in this model.
Main Methods:
- Intracranial inoculation of RSA59 in mice.
- Analysis of microglia activation markers (e.g., Iba1, CD11b, CD68).
- Affymetrix Microarray analysis for mRNA expression.
- Protein analysis of spinal cord extracts for inflammatory mediators (e.g., IFN-γ, IL-12).
Main Results:
- RSA59 infection led to significant upregulation of microglia/macrophage markers (Iba1, CD11b, CD68) and inflammatory mediators (IFN-γ, IL-12, mKC).
- Activated microglia and inflammatory mediators were associated with viral replication and IFN-γ production.
- These factors contribute to myelin sheath phagocytosis and demyelination.
Conclusions:
- Activated microglia and associated inflammatory mediators are key players in RSA59-induced CNS pathology.
- The local CNS microenvironment influences viral replication and immune responses during acute infection.
- This process leads to demyelination through phagocytosis of the myelin sheath.
Related Concept Videos
01:29Immune Response Against Viral Pathogens
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
01:30Inhibitors of Viral Protein Synthesis