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Updated: Aug 17, 2026
Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Mouse hepatitis virus 3 binding to macrophages correlates with resistance to experimental infection
C A Pereira1, C Moreira, M H Tsuhako
1Laboratório de Imunologia Viral, Instituto Butantan, Sao Paulo, Brazil. grugel@butantan.gov.br
Abstract:
Mouse hepatitis virus 3 (MHV3) infection of A/J and BALB/c mice has been used as a model of resistance/susceptibility. A/J mice recover from a mild disease after 4-6 days of infection and the BALB/c mice develop an acute hepatitis and die after 3-4 days of infection. In view of studying the MHV3 binding to cells or cell extracts, we performed an enzyme-linked immunosorbent assay-like virus-binding assay, preparing microplates with L929 cells, A/J or BALB/c mouse macrophages and also with proteins extracted from these cells. Higher MHV3 bindings were observed to proteins of BALB/c macrophages than to the A/J ones. The interferon-gamma (IFN-gamma) activation led to a reduction of MHV3 binding only to proteins of resistant A/J mouse macrophages. Our experiments contribute to the hypothesis that IFN-gamma activation of macrophages plays an important role against MHV3 infection by downregulating the expression of viral receptors.
Insights
Mouse hepatitis virus 3 (MHV3) infection susceptibility varies between mouse strains. Interferon-gamma activation reduces viral binding in resistant mice, suggesting a key role in controlling MHV3 infection.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Mouse hepatitis virus 3 (MHV3) infection models in A/J (resistant) and BALB/c (susceptible) mice reveal differential disease outcomes.
- A/J mice recover from mild MHV3 infection, while BALB/c mice succumb to acute hepatitis.
- Investigating MHV3 binding mechanisms using virus-binding assays with L929 cells, macrophages, and cell extracts.
Discussion:
- MHV3 exhibited higher binding affinity to proteins from susceptible BALB/c macrophages compared to resistant A/J macrophages.
- Interferon-gamma (IFN-gamma) activation significantly reduced MHV3 binding exclusively to proteins from resistant A/J mouse macrophages.
- These findings support the hypothesis that IFN-gamma activation of macrophages is crucial for combating MHV3 infection.
Key Insights:
- Differential binding of MHV3 to macrophage proteins correlates with mouse strain resistance/susceptibility.
- IFN-gamma activation modulates viral receptor expression, impacting MHV3 infectivity.
- Macrophage-mediated antiviral mechanisms are central to MHV3 resistance.
Outlook:
- Further research into specific viral receptors and IFN-gamma signaling pathways in MHV3 infection.
- Exploring therapeutic strategies targeting macrophage activation for MHV3 treatment.
- Translating findings to understand host-pathogen interactions in other viral diseases.
