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Oncolytic vesicular stomatitis virus expressing interferon-γ has enhanced therapeutic activity

Marie-Claude Bourgeois-Daigneault1, Dominic Guy Roy1, Theresa Falls2

  • 1Ottawa Hospital Research Institute, Centre for Innovative Cancer Research, Ottawa, Ontario, Canada; University of Ottawa, Biochemistry, Microbiology and Immunology Department, Ottawa, Ontario, Canada.

Molecular Therapy Oncolytics
|April 28, 2016
PubMed

Insights

Engineered oncolytic viruses expressing interferon-gamma (IFN-γ) enhance antitumor immunity. This immunotherapy approach activates immune cells, slows tumor growth, and prolongs survival in preclinical models.

Area of Science:

  • Immunology
  • Virology
  • Cancer Therapy

Background:

  • Oncolytic viruses stimulate antitumor immune responses through tumor cell replication.
  • Immunotherapy, particularly using oncolytic viruses, is a rapidly advancing field.
  • Durable patient responses to oncolytic virotherapy are linked to immune stimulation.

Purpose of the Study:

  • To engineer vesicular stomatitis virus (VSV) to express the proinflammatory cytokine interferon-gamma (IFN-γ).
  • To evaluate the immunomodulatory and therapeutic effects of the engineered IFN-γ-encoding VSV in murine tumor models.
  • To elucidate the immune-mediated mechanisms underlying the enhanced efficacy of the engineered oncolytic virus.

Main Methods:

  • Engineering VSV to encode IFN-γ.
  • Treatment of 4T1 mammary adenocarcinoma and other murine tumor models with engineered and parental VSV.
  • Characterization of immune responses, including dendritic cell activation and cytokine secretion.
  • Assessment of therapeutic outcomes: tumor growth, metastasis, and survival.
  • Evaluation of efficacy in immunocompromised animal models.

Main Results:

  • The IFN-γ-encoding VSV demonstrated enhanced activation of dendritic cells compared to the parental virus.
  • Treatment with the engineered virus led to increased secretion of proinflammatory cytokines.
  • The IFN-γ virus significantly slowed tumor growth and reduced lung metastasis in multiple models.
  • Survival was prolonged in tumor-bearing animals treated with the engineered virus.
  • Therapeutic efficacy was dependent on an intact immune system, suggesting a T-cell-mediated mechanism.

Conclusions:

  • Engineered oncolytic viruses can serve as potent immune stimulators to enhance antitumor immunity.
  • Targeted gene therapy with oncolytic viruses encoding cytokines like IFN-γ offers a promising strategy for cancer treatment.
  • The T-cell-mediated immune response is crucial for the therapeutic benefits of this oncolytic virus approach.
  • VSV engineered to express IFN-γ exhibits significant preclinical antitumor activity.

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