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An oncolytic herpesvirus expressing E-cadherin improves survival in mouse models of glioblastoma

Bo Xu1,2, Rui Ma2, Luke Russell2

  • 1Division of Hematology, Department of Internal Medicine, College of Medicine, The Ohio State University, Columbus, Ohio, USA.

Nature Biotechnology
|November 27, 2018
PubMed

Insights

Engineered oncolytic herpes simplex virus (oHSV) expressing E-cadherin improved glioblastoma treatment by enhancing viral spread and reducing immune clearance. This strategy shows promise for improving cancer virotherapy efficacy.

Area of Science:

  • Oncology
  • Virology
  • Immunology

Background:

  • Oncolytic virus therapy efficacy is limited by immune cell clearance and poor tumor spread.
  • Natural killer (NK) cells contribute to viral clearance, while poor viral spread hinders intratumoral efficacy.

Purpose of the Study:

  • To engineer an oncolytic herpes simplex virus (oHSV) to overcome immune clearance and enhance intratumoral spread.
  • To evaluate the efficacy of the engineered oHSV expressing E-cadherin in glioblastoma models.

Main Methods:

  • Engineered oHSV to express CDH1 (E-cadherin), a molecule that binds to the KLRG1 receptor on NK cells.
  • Assessed E-cadherin expression, viral spread, and NK cell interactions in vitro.
  • Evaluated in vivo efficacy in glioblastoma-bearing mouse models.

Main Results:

  • Engineered oHSV (OV-CDH1) induced E-cadherin expression on glioblastoma cells, facilitating cell-to-cell infection and viral spread.
  • Ectopic E-cadherin protected infected cells from KLRG1+ NK cell-mediated killing.
  • OV-CDH1 treatment significantly improved survival in mouse models, mainly due to enhanced viral spread.

Conclusions:

  • Virus-induced E-cadherin expression is a viable strategy to improve oncolytic virotherapy.
  • This approach enhances viral spread and reduces immune clearance, offering a generalizable method for cancer virotherapy.

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