Recent studies based on animal models have shown the advantages and potential of oncolytic viral
therapy using HSV-1 -based replication-competent vectors in the treatment of liver
tumors, but little is known about the cellular targets that are modulated during
viral infection. In the present work, we have studied the effects of intratumoral
injections of HSV-1 Cgal(+) strain in a murine model of human
hepatoma xenografts. Viral replication was assessed for more than 1month, leading to a significant reduction of
tumor growth rate mediated, in part, by a
cyclin B dependent cell proliferation arrest. Early events resulting in this effect were analyzed using a proteomic approach.
Protein extracts from xenografted human
hepatomas treated with saline or HSV-1 Cgal(+) strain during 24h were compared by 2-D DIGE and differential spots were identified by nanoLC-ESI-MS/MS. Alterations on
glutathione S transferase 1 Omega, and ERp29 suggest novel HSV-1 Cgal(+) targets in solid liver
tumors. Additionally, ERp29 showed a complex differential
isoform pattern upon HSV-1 Cgal(+)
infection, suggesting regulatory mechanisms based on post-translational modification events.