biostudies-literatureJanelle VCanadian Institutes of Health Research1198-1210https://www.ebi.ac.uk/biostudies/studies/S-EPMC4048893biostudies-literatureUnknown22(6)Cancer therapy using oncolytic viruses has gained interest in the last decade. Vesicular stomatitis virus is an attractive candidate for this alternative treatment approach. The importance of the immune response against tumor antigens in virotherapy efficacy is now well recognized, however, its relative contribution versus the intrinsic oncolytic capacity of viruses has been difficult to evaluate. To start addressing this question, we compared glycoprotein and matrix mutants of vesicular stomatitis virus (VSV), showing different oncolytic potentials for B16/B16gp33 melanoma tumor cells in vitro, with the wild-type virus in their ability to induce tumor-specific CD8(+) T cell responses and control tumor progression in vivo. Despite the fact that wild-type and G mutants induced a stronger gpMolecular therapy : the journal of the American Society of Gene TherapyThe strength of the T cell response against a surrogate tumor antigen induced by oncolytic VSV therapy does not correlate with tumor control.PMC4048893MOP-89797Lamarre APoliquin LJanelle VLanglois MPCharpentier TLapierre PfalseThe strength of the T cell response against a surrogate tumor antigen induced by oncolytic VSV therapy does not correlate with tumor control.Cancer therapy using oncolytic viruses has gained interest in the last decade. Vesicular stomatitis virus is an attractive candidate for this alternative treatment approach. The importance of the immune response against tumor antigens in virotherapy efficacy is now well recognized, however, its relative contribution versus the intrinsic oncolytic capacity of viruses has been difficult to evaluate. To start addressing this question, we compared glycoprotein and matrix mutants of vesicular stomatitis virus (VSV), showing different oncolytic potentials for B16/B16gp33 melanoma tumor cells in vitro, with the wild-type virus in their ability to induce tumor-specific CD8(+) T cell responses and control tumor progression in vivo. Despite the fact that wild-type and G mutants induced a stronger gp2014-01-01T00:00:00Z2014 Jun2025-04-19T14:54:16.52Z2019-03-27T01:29:40ZS-EPMC40488932459004710.1038/mt.2014.34