IL4 and helminthiasis: Because our previous work indicated that challenge with HP during MHV68 latency increased in vivo reactivation in a STAT6-dependent manner [7] and peritoneal macrophages respond to IL-4 signaling leading to proliferation and activation of STAT6 dependent gene expression [13,22], we examined whether increased virus reactivation in mice with preexisting helminth infection required STAT6 signaling.