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Updated: May 1, 2026
A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Characterization of chikungunya virus induced host response in a mouse model of viral myositis
Rekha Dhanwani1, Mohsin Khan1, Vinay Lomash2
1Department of Virology, Defence Research & Development Establishment (DRDE), Gwalior, India.
Abstract:
While a number of studies have documented the persistent presence of chikungunya virus (CHIKV) in muscle tissue with primary fibroblast as the preferable cell target, little is known regarding the alterations that take place in muscle tissue in response to CHIKV infection. Hence, in the present study a permissive mouse model of CHIKV infection was established and characterized in order to understand the pathophysiology of the disease. The two dimensional electrophoresis of muscle proteome performed for differential analysis indicated a drastic reprogramming of the proteins from various classes like stress, inflammation, cytoskeletal, energy and lipid metabolism. The roles of the affected proteins were explained in relation to virus induced myopathy which was further supported by the histopathological and behavioural experiments proving the lack of hind limb coordination and other loco-motor abnormalities in the infected mice. Also, the level of various pro-inflammatory mediators like IL-6, MCP-1, Rantes and TNF-α was significantly elevated in muscles of infected mice. Altogether this comprehensive study of characterizing CHIKV induced mouse myopathy provides many potential targets for further evaluation and biomarker study.
Insights
Chikungunya virus (CHIKV) infection causes significant muscle tissue changes, including protein reprogramming and inflammation, leading to virus-induced myopathy in mice. This study identifies potential targets for future chikungunya research and biomarker development.
Area of Science:
- Virology
- Immunology
- Pathophysiology
Background:
- Chikungunya virus (CHIKV) persists in muscle tissue, targeting fibroblasts.
- Limited understanding of CHIKV-induced muscle tissue alterations and resulting myopathy.
Purpose of the Study:
- Establish and characterize a permissive mouse model for CHIKV infection.
- Investigate the pathophysiology of CHIKV-induced myopathy.
Main Methods:
- Two-dimensional electrophoresis for differential proteome analysis of muscle tissue.
- Histopathological and behavioral assessments in infected mice.
- Quantification of pro-inflammatory mediators (IL-6, MCP-1, Rantes, TNF-α).
Main Results:
- Significant reprogramming of muscle proteins involved in stress, inflammation, cytoskeleton, and metabolism.
- Evidence of virus-induced myopathy, including impaired hind limb coordination and loco-motor abnormalities.
- Elevated levels of key pro-inflammatory mediators in infected muscle tissue.
Conclusions:
- CHIKV infection induces widespread muscle protein alterations and inflammation, causing myopathy.
- The characterized mouse model is valuable for studying CHIKV pathophysiology.
- Identified protein changes and inflammatory mediators represent potential therapeutic targets and biomarkers.
