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Vesicular Stomatitis Virus (VSV) Therapy of Tumors
Author(s) -
Balachandran Siddharth,
Barber Glen N.
Publication year - 2000
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/713803696
Subject(s) - vesicular stomatitis virus , virology , biology , cytolysis , protein kinase r , interferon , oncolytic virus , vesicular stomatitis indiana virus , virus , viral replication , rna , vesicular stomatitis , rhabdoviridae , rna virus , in vitro , kinase , protein kinase a , microbiology and biotechnology , cytotoxicity , cyclin dependent kinase 2 , gene , biochemistry
Abstract Vesicular stomatitis virus (VSV) is an essentially nonpathogenic negative‐stranded RNA virus, the replication of which is extremely sensitive to the antiviral effects of interferon (IFN). We demonstrate here that VSV selectively induces the cytolysis of numerous transformed human cell lines in vitro, with all the morphological characteristics of apoptotic cell death. Importantly, VSV can also potently inhibit the growth of p53‐null C6 glioblastoma tumors in vivo without infecting and replicating in normal tissue. With our previous findings demonstrating that primary cells containing the double‐stranded RNA‐activated protein kinase PKR and a functional IFN system are not permissive to VSV replication, these results suggest that signaling by IFN may be defective in many malignancies. Thus VSV might be useful in novel therapeutic strategies for targeting neoplastic disease.