This pathogen, which causes high fevers and severe joint pain, triggered a recent epidemic in Southeast Asia, infecting more than 30% of the population in some areas.
A team led by Marc Lecuit and Matthew Albert at the Pasteur Institute in Paris found that individuals infected with Chikungunya virus had increased levels of type I IFNs in their blood. But the source of the virus-fighting IFN proteins came as a surprise.
Viruses related to Chikungunya trigger type I IFN production mostly from immune cells. But during Chikungunya infection, immune cells neither produced nor responded to type I IFNs. Rather non-immune cells called fibroblasts—the main target of virus infection—provided the essential type I IFN.
This unique feature should be taken into consideration in future efforts to develop therapeutic strategies for controlling Chikungunya virus infection.About The Journal of Experimental Medicine
Schilte, C., et al. 2010. J. Exp. Med. doi:10.1084/jem.20090851.
Rita Sullivan | EurekAlert!
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