The cytokine, Interleukin 27 (IL-27), may be the key to fighting and treating respiratory syncytial virus (RSV) infections, according to research from University of Pennsylvania.

Working with a mouse-model of parainfluenza virus infection, Sendai virus, which causes similar symptoms and patterns of tissue damage to RSV, researchers found that mice fared much worse in fighting the infection when their cells lacked IL-27 signaling.

When the researchers blocked IL-27 signaling – by genetically engineering mice to lack working IL-27 receptors or IL-27 proteins – infected mice suffered much worse illness and higher mortality.