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Updated: May 8, 2026

Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo
12:42

Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo

Published on: January 7, 2019

Oncolytic vesicular stomatitis virus as a treatment for neuroendocrine tumors

Reese W Randle1, Scott A Northrup, S Joseph Sirintrapun

  • 1Department of General Surgery, Wake Forest School of Medicine, Winston-Salem, NC.

Surgery
|August 27, 2013
PubMed
Abstract

Insights

Vesicular stomatitis virus (VSV) effectively infects and kills neuroendocrine tumor (NET) cells by exploiting their defective antiviral response. This makes M51R-VSV a promising oncolytic virus therapy for advanced NETs.

Area of Science:

  • Oncolytic virotherapy
  • Cancer biology
  • Immunology

Background:

  • Neuroendocrine tumors (NETs) pose therapeutic challenges, with limited options for non-operable cases.
  • Malignancies often develop defective antiviral responses, presenting a potential therapeutic vulnerability.
  • Recombinant vesicular stomatitis virus (VSV) was investigated for its potential to target NETs.

Purpose of the Study:

  • To evaluate the efficacy of wild-type VSV and an attenuated mutant (M51R-VSV) against human NET cell lines.
  • To identify and characterize the defective antiviral pathways in NET cells.
  • To assess the in vivo therapeutic potential of M51R-VSV in murine xenograft models.

Main Methods:

  • Infection and lethality assays were performed on human NET cell lines (H727, UMC-11, CNDT2.5).
  • Beta-interferon (IFN-β) pathway activation was assessed post-infection.
  • Murine xenografts received intratumoral injections of M51R-VSV to evaluate in vivo efficacy.

Main Results:

  • VSV rapidly infected (>99% in 24h) and killed (>95% in 72h) NET cells.
  • NET cells exhibited deficient IFN-β production, rendering them susceptible to VSV-induced oncolysis.
  • M51R-VSV treatment significantly suppressed tumor growth in all tested xenograft models (P < .001).

Conclusions:

  • VSV effectively targets and eliminates human NETs by exploiting their impaired type I antiviral response.
  • The attenuated M51R-VSV demonstrates significant anti-tumor activity in vivo.
  • M51R-VSV represents a promising oncolytic virus candidate for advanced NET treatment.

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