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In recent years, oncolytic virotherapy has emerged as an altemative therapy against cancer showing great potential. Oncolytic tumor regression in vivo has been shown to be a multifactorial process involving viral gene expression and direct celi lysis, as well as the recruitment of immune effector cells directed against infected tumor cells (Diaz et al., 2007; Galivo et al., 2009; Prestwich et al., 2009; Toda et al., 1999; Wongthida et al., 2010). A well-characterized oncolytic virus being developed for such purpose is the prototypie Rhabdoviridae vesicular stomatitis virus (VSV) VSV possesses intrinsic oncolytic properties sińce it replicates morę efficiently in type-I interferon-defective cells, a pathway ffequently impaired during tumorigenesis (Naik and Russell, 2009; Stojdl et al., 2000). Several successfiil preclinical and clinical studies against prostatę, breast, colorectal and liver cancers (Ahmed et al., 2010; Chang et al., 2010; Heo et al., 2013b; Huang et al., 2003), as well as melanoma (Femandez et al., 2002) and glioblastoma (Ozduman et al., 2008) indicate that VSV oncolytic therapy is a promising altemative treatment against a number of cancer types. In addition to the direct lysis of cancer cells, VSV treatment also generates a CD8⁺ T celi dependent tumor-specific immune response that is induced following the release of tumor antigens by infected cells in a proinflammatory environment (Diaz et al., 2007). However, this tumor-specific immune response generated following VSV treatment is usually weak and leads only to a partial control of tumor growth. Hence, the causes for the high variability in the outeomes of VSV oncolytic therapy need to be better understood (Rommelfanger et al., 2012).