ArticleMolecular therapy oncolytics2017
Targeting an Oncolytic Influenza A Virus to Tumor Tissue by Elastase.
Article in Molecular therapy oncolytics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Synthetic Biology Strategies for the Development of Live Attenuated Influenza Viruses: Recent Advances and Applications.Viruses · 2026Review
- Design and Efficacy of Oncolytic Viruses and Antitumor Vaccines: A Dead End in the Immunotherapy of Pancreatic Cancer?International journal of molecular sciences · 2025Review
- New characteristics of cancer immunotherapy: trends in viral tumor immunotherapy with influenza virus-based approaches.Journal of Zhejiang University. Science. B · 2025Review
- Tutorial: design, production and testing of oncolytic viruses for cancer immunotherapy.Nature protocols · 2024Review
- Progression of oncolytic virus in liver cancer treatment.Frontiers in oncology · 2024Review
- Immune responses elicited by ssRNA(-) oncolytic viruses in the host and in the tumor microenvironment.Journal of cancer metastasis and treatment · 2023Article
- Oncolytic Activity of a Chimeric Influenza A Virus Carrying a Human CTLA4 Antibody in Hepatocellular Carcinoma.Frontiers in oncology · 2022Article
- Development and application of reverse genetic technology for the influenza virus.Virus genes · 2021Review
- From threat to cure: understanding of virus-induced cell death leads to highly immunogenic oncolytic influenza viruses.Cell death discovery · 2020Review
- Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncolytic viruses are currently established as a novel type of immunotherapy. The challenge is to safely target oncolytic viruses to tumors. Previously, we have generated influenza A viruses (IAVs) containing deletions in the viral interferon antagonist. Those deletions have attenuated the virus in normal tissue but allowed replication in tumor cells. IAV entry is mediated by hemagglutinin (HA), which needs to be activated by a serine protease, for example, through trypsin. To further target the IAV to tumors, we have changed the trypsin cleavage site to an elastase cleavage site. We chose this cleavage site because elastase is expressed in the tumor microenvironment. Moreover, the exchange of the cleavage site previously has been shown to attenuate viral growth in lungs. Newly generated elastase-activated influenza viruses (AE viruses) grew to similar titers in tumor cells as the trypsin-activated counterparts (AT viruses). Intratumoral injection of AE viruses into syngeneic B16f1 melanoma-derived tumors in mice reduced tumor growth similar to AT viruses and had a better therapeutic effect in heterologous human PANC-1-derived tumors. Therefore, the introduction of the attenuation marker "elastase cleavage site" in viral HA allows for safe, effective oncolytic virus therapy.
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