ArticleMolecular therapy oncolytics2021
Activation of interferon regulatory factor 3 by replication-competent vaccinia viruses improves antitumor efficacy mediated by T cell responses.
Article in Molecular therapy oncolytics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Identification and evaluation of novel intergenic sites in the vaccinia virus genome for transgene insertion.Molecular therapy. Oncology · 2026Article
- Oncolytic immunovirotherapy: finding the tumor antigen needle in the antiviral haystack.Immunotherapy · 2025Review
- A new MVA ancestor-derived oncolytic vaccinia virus induces immunogenic tumor cell death and robust antitumor immune responses.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Molecular Circuits of Immune Sensing and Response to Oncolytic Virotherapy.International journal of molecular sciences · 2024Review
- Tumor Tropism of DNA Viruses for Oncolytic Virotherapy.Viruses · 2023Review
- Improving poxvirus-mediated antitumor immune responses by deleting viral cGAMP-specific nuclease.Cancer gene therapy · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, oncolytic vaccinia viruses (VACVs) have shown their potential to provide for clinically effective cancer treatments. The reason for this clinical usefulness is not only the direct destruction of infected cancer cells but also activation of immune responses directed against tumor antigens. For eliciting a robust antitumor immunity, a dominant T helper 1 (Th1) cell differentiation of the response is preferred, and such polarization can be achieved by activating the Toll-like receptor 3 (TLR3)-interferon regulatory factor 3 (IRF3) signaling pathway. However, current VACVs used as oncolytic viruses to date still encode several immune evasion proteins involved in the inhibition of this signaling pathway. By inactivating genes of selected regulatory virus proteins, we aimed for a candidate virus with increased potency to activate cellular antitumor immunity but at the same time with a fully maintained replicative capacity in cancer cells. The removal of up to three key genes (
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Registered trials
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