Antiapoptotic mechanisms early in infection may facilitate enhanced viral replication and possibly increased therapeutic efficacy, and several other studies have shown VACV’s ability to inhibit apoptosis.15,16 In a recent study assessing the permissivity of cell lines to GLV-1h68, casp3 was initially downregulated, again suggesting that antiapoptosis may help facilitate viral replication.11 This evidence concerns the gene CASP3 and infection.