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Mouse macrophage innate immune response to chikungunya virus infection

Shiril Kumar1, Marie-Christine Jaffar-Bandjee12, Claude Giry1, Léa Connen de Kerillis1, Andres Merits3, Philippe Gasque1 and Jean-Jacques Hoarau14*

Author Affiliations

1 GRI/IRG (EA4517), Immunopathology and infectious diseases research grouping, University of La Reunion, CHU and CYROI research centres, St-Denis, La Reunion, France

2 Microbiology/Virology laboratory, CHU Félix-Guyon, F-97400, Saint-Denis, La Reunion, France

3 Institute of Technology, University of Tartu, Tartu, Estonia

4 GRI – (EA4517) Université de la Réunion, Recherche – RDC, CHU Félix-Guyon, Bellepierre, 97405, Saint-Denis cedex, Ile de la Réunion, France (DOM

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Virology Journal 2012, 9:313  doi:10.1186/1743-422X-9-313

Published: 19 December 2012



Infection with Chikungunya alphavirus (CHIKV) can cause severe arthralgia and chronic arthritis in humans with persistence of the virus in perivascular macrophages of the synovial membrane by mechanisms largely ill-characterized.


We herein analysed the innate immune response (cytokine and programmed cell death) of RAW264.7 mouse macrophages following CHIKV infection. We found that the infection was restrained to a small percentage of cells and was not associated with a robust type I IFN innate immune response (IFN-α4 and ISG56). TNF-α, IL-6 and GM-CSF expression were upregulated while IFN-γ, IL-1α, IL-2, IL-4, IL-5, IL-10 or IL-17 expression could not be evidenced prior to and after CHIKV exposure. Although CHIKV is known to drive apoptosis in many cell types, we found no canonical signs of programmed cell death (cleaved caspase-3, -9) in infected RAW264.7 cells.


These data argue for the capacity of CHIKV to infect and drive a specific innate immune response in RAW264.7 macrophage cell which seems to be polarized to assist viral persistence through the control of apoptosis and IFN signalling.

Chikungunya virus; Macrophage; Apoptosis; Viral persistence; Inflammation