To investigate the role of Ly6Chi inflammatory monocytes in control of RRV-T48-nsP16M infection, we used transgenic CCR2 depleter mice in which the CCR2 locus was modified to place a simian diphtheria toxin receptor (DTR) and enhanced cyan fluorescent protein (CFP), separated by an aphthovirus 2A cleavage site, under control of the endogenous CCR2 promoter (CCR2-DTR) [59]. Here, HBEGF is linked to infection.