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Updated: Jun 9, 2025
Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
Comparison of Chikungunya Virus-Induced Disease Progression and Pathogenesis in Type-I Interferon Receptor-Deficient
Victoria A Graham1, Linda Easterbrook1, Emma Rayner1
1UK Health Security Agency (UKHSA), Porton Down, Salisbury SP4 0JG, Wiltshire, UK.
Abstract:
Chikungunya virus (CHIKV) is a mosquito-borne alphavirus causing a debilitating febrile illness with rheumatic disease symptoms of arthralgia and arthritis. Since its spread outside of Africa in 2005, it continues to cause outbreaks and disseminates into new territories. Intervention strategies are urgently required, including vaccination and antiviral approaches. To test efficacy, the use of small animal models is required. Two mouse strains, A129, with a deficiency in their type-I interferon (IFN) receptor, and C57BL/6 are widely used. A direct comparison of these strains alongside the wild-type parental strain of the A129 mice, 129Sv/Ev, was undertaken to assess clinical disease progression, viral loads in key tissues, histological changes and levels of sera biomarkers. Our results confirm the severe disease course in A129 mice which was not observed in the parental 129Sv/Ev strain. Of the two wild-type strains, viral loads were higher in 129Sv/Ev mice compared to C57BL/6 counterparts. Our results have established these models and parameters for the future testing of vaccines and antiviral approaches.
Insights
This study compared mouse models for Chikungunya virus (CHIKV) research. A129 mice showed severe disease, while 129Sv/Ev mice had higher viral loads than C57BL/6 mice, establishing parameters for vaccine and antiviral testing.
Area of Science:
- Virology
- Immunology
- Pathology
Background:
- Chikungunya virus (CHIKV) causes debilitating rheumatic disease and is spreading globally.
- Urgent need for effective vaccines and antiviral therapies.
- Small animal models are crucial for testing interventions.
Purpose of the Study:
- To directly compare disease progression, viral loads, and biomarkers in three mouse strains: A129, C57BL/6, and 129Sv/Ev.
- To establish reliable parameters for evaluating CHIKV countermeasures.
- To assess the suitability of different mouse models for CHIKV research.
Main Methods:
- Direct comparison of A129 (Type-I IFN receptor deficient), C57BL/6 (wild-type), and 129Sv/Ev (parental wild-type) mice.
- Assessment of clinical disease, viral loads in tissues, histological changes, and serum biomarkers.
- Chikungunya virus (CHIKV) infection model.
Main Results:
- A129 mice exhibited severe disease, unlike the parental 129Sv/Ev strain.
- Wild-type 129Sv/Ev mice showed higher viral loads compared to C57BL/6 mice.
- Established distinct disease profiles and viral dissemination patterns across the tested strains.
Conclusions:
- The A129 mouse model is highly susceptible to CHIKV, demonstrating severe pathology.
- 129Sv/Ev and C57BL/6 mice offer different but valuable models for studying CHIKV infection.
- These findings provide a foundation for selecting appropriate mouse models and parameters for future CHIKV vaccine and antiviral studies.
