ArticleMolecular therapy. Oncology2024
Virus replication is not required for oncolytic bovine herpesvirus-1 immunotherapy.
Article in Molecular therapy. Oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Oncolytic bovine herpesvirus type 1 induces immune microenvironment remodeling and enhances treatment responses in multiple myeloma.Haematologica · 2026Article
- Extracellular Vesicles Released by Bovine Alphaherpesvirus 1-Infected A549 Cells May Limit Subsequent Infections of the Progeny Virus.International journal of molecular sciences · 2025Article
- Enhanced potency of immune checkpoint inhibitors against poorly immunological solid tumors by immune stimulatory oncolytic adenoviruses-mediated remodeling of the tumor microenvironment.Molecular medicine (Cambridge, Mass.) · 2025Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncolytic viruses are a promising approach for cancer treatment where viruses selectively target and kill cancer cells while also stimulating an immune response. Among viruses with this ability, bovine herpesvirus-1 (BoHV-1) has several advantages, including observations suggesting it may not require viral replication for its anti-cancer effects. We previously demonstrated that binding and penetration of enveloped virus particles are sufficient to trigger intrinsic and innate immune signaling in normal cells, while other groups have published the efficacy of non-replicating viruses as viable immunotherapies in different cancer models. In this work, we definitively show that live and UV-inactivated (UV) (non-replicating) BoHV-1-based regimens extend survival of tumor-bearing mice to similar degrees and induce infiltration of similar immune cell populations, with the exception of neutrophils. Transcriptomic analysis of tumors treated with either live or UV BoHV-1-based regimens revealed similar pathway enrichment and a subset of overlapping differentially regulated genes, suggesting live and UV BoHV-1 have similar mechanisms of activity. Last, we present a gene signature across our
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