An oncolytic HSV-1 vector induces a therapeutic adaptive immune response against glioblastoma.


Journal

Journal of translational medicine
ISSN: 1479-5876
Titre abrégé: J Transl Med
Pays: England
ID NLM: 101190741

Informations de publication

Date de publication:
27 Sep 2024
Historique:
received: 01 08 2024
accepted: 04 09 2024
medline: 28 9 2024
pubmed: 28 9 2024
entrez: 28 9 2024
Statut: epublish

Résumé

Glioblastoma (GBM) is the most frequent and aggressive brain tumor in adults with the lowest survival rates five years post-diagnosis. Oncolytic viruses (OVs) selectively target and damage cancer cells, and for this reason they are being investigated as new therapeutic tools also against GBM. An oncolytic herpes simplex virus type 1 (oHSV-1) with deletions in the γ34.5 neurovirulence gene and the US12 gene, expressing enhanced green fluorescent protein (EGFP-oHSV-1) as reporter gene was generated and tested for its capacity to infect and kill the murine GL261 glioblastoma (GBM) cell line. Syngeneic mice were orthotopically injected with GL261cells. Seven days post-implantation, EGFP-oHSV-1 was administered intratumorally. Twenty-one days after parental tumor challenge in the opposite brain hemisphere, mice were sacrified and their brains were analysed by immunohistochemistry to assess tumor presence and cell infiltrate. oHSV-1 replicates and induces cell death of GL261 cells in vitro. A single intracranial injection of EGFP-oHSV-1 in established GL261 tumors significantly prolongs survival in all treated mice compared to placebo treatment. Notably, 45% of treated mice became long-term survivors, and rejected GL261 cells upon rechallenge in the contralateral brain hemisphere, indicating an anamnestic antitumoral immune response. Post-mortem analysis revealed a profound modification of the tumor microenvironment with increased infiltration of CD4 + and CD8 + T lymphocytes, intertumoral vascular collapse and activation and redistribution of macrophage, microglia, and astroglia in the tumor area, with the formation of intense fibrotic tissue suggestive of complete rejection in long-term survivor mice. EGFP-oHSV1 demonstrates potent antitumoral activity in an immunocompetent GBM model as a monotherapy, resulting from direct cell killing combined with the stimulation of a protective adaptive immune response. These results open the way to possible application of our strategy in clinical setting.

Sections du résumé

BACKGROUND BACKGROUND
Glioblastoma (GBM) is the most frequent and aggressive brain tumor in adults with the lowest survival rates five years post-diagnosis. Oncolytic viruses (OVs) selectively target and damage cancer cells, and for this reason they are being investigated as new therapeutic tools also against GBM.
METHODS METHODS
An oncolytic herpes simplex virus type 1 (oHSV-1) with deletions in the γ34.5 neurovirulence gene and the US12 gene, expressing enhanced green fluorescent protein (EGFP-oHSV-1) as reporter gene was generated and tested for its capacity to infect and kill the murine GL261 glioblastoma (GBM) cell line. Syngeneic mice were orthotopically injected with GL261cells. Seven days post-implantation, EGFP-oHSV-1 was administered intratumorally. Twenty-one days after parental tumor challenge in the opposite brain hemisphere, mice were sacrified and their brains were analysed by immunohistochemistry to assess tumor presence and cell infiltrate.
RESULTS RESULTS
oHSV-1 replicates and induces cell death of GL261 cells in vitro. A single intracranial injection of EGFP-oHSV-1 in established GL261 tumors significantly prolongs survival in all treated mice compared to placebo treatment. Notably, 45% of treated mice became long-term survivors, and rejected GL261 cells upon rechallenge in the contralateral brain hemisphere, indicating an anamnestic antitumoral immune response. Post-mortem analysis revealed a profound modification of the tumor microenvironment with increased infiltration of CD4 + and CD8 + T lymphocytes, intertumoral vascular collapse and activation and redistribution of macrophage, microglia, and astroglia in the tumor area, with the formation of intense fibrotic tissue suggestive of complete rejection in long-term survivor mice.
CONCLUSIONS CONCLUSIONS
EGFP-oHSV1 demonstrates potent antitumoral activity in an immunocompetent GBM model as a monotherapy, resulting from direct cell killing combined with the stimulation of a protective adaptive immune response. These results open the way to possible application of our strategy in clinical setting.

Identifiants

pubmed: 39334370
doi: 10.1186/s12967-024-05650-5
pii: 10.1186/s12967-024-05650-5
doi:

Substances chimiques

Green Fluorescent Proteins 147336-22-9
enhanced green fluorescent protein 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

862

Subventions

Organisme : Fondazione AIRC per la ricerca sul cancro ETS
ID : IG 2021-ID.26195
Organisme : Fondazione Celeghin
ID : Fondazione Celeghin
Organisme : Giancarlo Balbinot (Isopak Srl Unipersonale)
ID : Giancarlo Balbinot (Isopak Srl Unipersonale)

Informations de copyright

© 2024. The Author(s).

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Auteurs

Alberto Reale (A)

Department of Molecular Medicine, University of Padua, Padua, 35131, Italy.

Andrea Gatta (A)

Department of Medicine and Technological Innovation, University of Insubria, via O.Rossi 9, Varese, 21100, Italy.

Amruth Kaleem Basha Shaik (AKB)

Department of Medicine and Technological Innovation, University of Insubria, via O.Rossi 9, Varese, 21100, Italy.

Mariam Shallak (M)

Department of Medicine and Technological Innovation, University of Insubria, via O.Rossi 9, Varese, 21100, Italy.

Anna Maria Chiaravalli (AM)

Unit of Pathology, ASST Sette-Laghi, Varese, 21100, Italy.

Michele Cerati (M)

Unit of Pathology, ASST Sette-Laghi, Varese, 21100, Italy.

Martina Zaccaria (M)

Department of Medicine and Technological Innovation, University of Insubria, via O.Rossi 9, Varese, 21100, Italy.

Stefano La Rosa (S)

Department of Medicine and Technological Innovation, University of Insubria, via O.Rossi 9, Varese, 21100, Italy.
Unit of Pathology, ASST Sette-Laghi, Varese, 21100, Italy.

Arianna Calistri (A)

Department of Molecular Medicine, University of Padua, Padua, 35131, Italy.

Roberto Sergio Accolla (RS)

Department of Medicine and Technological Innovation, University of Insubria, via O.Rossi 9, Varese, 21100, Italy. Roberto.accolla@uninsubria.it.

Greta Forlani (G)

Department of Medicine and Technological Innovation, University of Insubria, via O.Rossi 9, Varese, 21100, Italy. greta.forlani@uninsubria.it.

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