ArticleMolecular therapy oncolytics2021
Deletion of immunomodulatory genes as a novel approach to oncolytic vaccinia virus development.
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 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Heterologous vaccination with a next-generation vaccinia virus and Ad26 induces Ebola-specific immunity in macaques.NPJ vaccines · 2026Article
- Oncolytic Viruses as a Novel Therapeutic Approach for Colorectal Cancer: Mechanisms, Current Advances, and Future Directions.Cancers · 2025Review
- Tutorial: design, production and testing of oncolytic viruses for cancer immunotherapy.Nature protocols · 2024Review
- Oncolytic Viruses in the Era of Omics, Computational Technologies, and Modeling: Thesis, Antithesis, and Synthesis.International journal of molecular sciences · 2023Review
- Tumor Tropism of DNA Viruses for Oncolytic Virotherapy.Viruses · 2023Review
- The employment of vaccinia virus for colorectal cancer treatment: A review of preclinical and clinical studies.Human vaccines & immunotherapeutics · 2022Review
- Comprehensive assessment on the applications of oncolytic viruses for cancer immunotherapy.Frontiers in pharmacology · 2022Review
- CRISPR-mediated rapid arming of poxvirus vectors enables facile generation of the novel immunotherapeutic STINGPOX.Frontiers in immunology · 2022Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vaccinia virus (VV) has emerged as a promising platform for oncolytic virotherapy. Many clinical VV candidates, such as the double-deleted VV, vvDD, are engineered with deletions that enhance viral tumor selectivity based on cellular proliferation rates. An alternative approach is to exploit the dampened interferon-based innate immune responses of tumor cells by deleting one of the many VV immunomodulatory genes expressed to dismantle the antiviral response. We hypothesized that such a VV mutant would be attenuated in non-tumor cells but retain the ability to effectively propagate in and kill tumor cells, yielding a tumor-selective oncolytic VV with significant anti-tumor potency. In this study, we demonstrated that VVs with a deletion in one of several VV immunomodulatory genes (N1L, K1L, K3L, A46R, or A52R) have similar or improved
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