The role of ICP0-Null HSV-1 and interferon signaling defects in the effective treatment of breast adenocarcinoma

摘要: Abstract Oncolytic viruses that selectively replicate in cancer cells have been described for over 50 years. Despite the observation by several groups multimutated herpes simplex type 1 vectors are oncolytic a variety of murine tumor models, potential ICP0 null mutants has not described. This study characterizes novel second-generation vector gene. We tested three mutant and found all were cytotoxic human vitro. Furthermore, we provide evidence mechanistic link between ICP0's function interferon signaling pathways observed capacity mutants. Using an immunocompetent model breast adenocarcinoma demonstrate KM100 completely eradicates tumors ∼80% treated animals significantly increases survival. Our data suggest active viral replication is necessary effective regression. In addition, characterized as anti-tumor vaccine since cured mice to elicit robust immune response refractory subsequent growth upon rechallenge.