Vesicular stomatitis virus (VSV) therapy of tumors

S. Balachandran, G. N. Barber

Research output: Contribution to journalArticlepeer-review

132 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)135-138
Number of pages4
JournalIUBMB life
Issue number2
StatePublished - Jan 1 2000


  • Interferon
  • Oncolytic virus
  • PKR
  • Tumor
  • VSV

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology


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