In a mouse model of MERS coronavirus (MERS-CoV) infection, type I IFN administration within 1 day after infection resulted in protection from lethal challenge, while delayed IFN-β treatment on PID 2 and 4 caused a significantly elevated expression of CCL2, increased infiltration of monocytes and neutrophils into the lungs, and development of fatal pneumonia in sublethally infected animals [58]. Here, CCL2 is linked to susceptibility to pneumonia measurement.