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Published on: October 17, 2018
Expression profile of immune response genes during acute myopathy induced by chikungunya virus in a mouse model
Dilip R Patil1, Supriya L Hundekar, Vidya A Arankalle
1National Institute of Virology, Microbial Containment Complex, 130/1 Sus Road, Pune 411021, India.
Abstract:
During the recent re-emergence of chikungunya, clinical complications and deaths were recorded. Persistent musculoskeletal pain, arthralgia, arthritis were among the most common complications. To understand pathogenesis of CHIKV induced disease, we developed suckling, outbred mouse model presenting with severe myopathology. Histopathology, dynamics of viral load, IgG antibodies/isotypes, serum cytokines by cytometric bead array and mRNA expression levels of immune response genes in the target tissue by Taqman Low Density Array were studied. Peak viral load was associated with peak serum levels of CCL-2,KC, CCL-4, RANTES, IL-6, IL-10, CSF-3, and locally very high mRNA expression of CCL-2, CXCL-10, CXCL-11 and concomitant IFNγ, IL-10, STAT-1, SOCS-1 and CSF-3 suggesting strong IFNγ program. Symptomatic phase correlated with peak serum levels of IL-2, IFNγ, IL-17, CCL-3, IL-1β, eotaxin, IL-9 and CSF-2 and locally with peak mRNA expression of macrophage induced pro inflammatory cytokines and immune infiltration biased towards Th1. IgG antibodies were detected on day 6PI, reaching high titres by day 11PI. IgG2a was the predominant isotype, indicating Th1 bias. This is the first report of comprehensive analysis of immune response genes expression in target tissue of CHIKV mouse model. The data would contribute significantly in understanding pathogenesis of CHIKV disease and viral myopathies.
Insights
This study reveals chikungunya virus (CHIKV) infection in mice causes severe muscle damage and a strong interferon-gamma (IFNγ) immune response. Understanding this pathogenesis aids in developing treatments for CHIKV-induced myopathy.
Area of Science:
- Virology
- Immunology
- Pathogenesis
Background:
- Chikungunya virus (CHIKV) re-emergence has led to severe clinical complications, including persistent musculoskeletal pain.
- Understanding the pathogenesis of CHIKV-induced disease is crucial for effective treatment strategies.
Purpose of the Study:
- To develop and characterize a suckling mouse model of CHIKV-induced myopathology.
- To comprehensively analyze the immune response and gene expression in the target tissue during CHIKV infection.
Main Methods:
- Development of a suckling mouse model for CHIKV infection.
- Analysis of viral load, IgG antibodies/isotypes, serum cytokines (cytometric bead array), and immune response gene mRNA expression (Taqman Low Density Array).
Main Results:
- Peak viral load correlated with elevated serum cytokines (CCL-2, IL-6, IL-10, etc.) and high local mRNA expression of IFNγ-related genes, indicating a strong IFNγ program.
- The symptomatic phase showed increased pro-inflammatory cytokines and Th1-biased immune infiltration.
- High titers of IgG antibodies, predominantly IgG2a, were detected, further supporting a Th1 immune bias.
Conclusions:
- This study presents the first comprehensive analysis of immune response gene expression in the target tissue of a CHIKV mouse model.
- The findings provide significant insights into the pathogenesis of CHIKV disease and viral myopathies.
- The developed mouse model is valuable for studying CHIKV-induced muscle pathology and immune responses.
