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Multiple myeloma remains a significant challenge in hematology due to persistent drug resistance and an immunosuppressive bone marrow microenvironment. Oncolytic virotherapy for myeloma has emerged as a dual-action approach that combines direct tumor cell lysis with robust immune activation. While human viruses often face hurdles from pre-existing immunity, researchers are now looking toward non-pathogenic animal viruses like bovine herpesvirus type 1 (BoHV-1). This virus selectively infects malignant plasma cells, triggering a cascade of anti-tumor events that could redefine standard care protocols.
BoHV-1 effectively enters myeloma cells and induces mitochondrial apoptosis. This process suppresses critical pro-survival programs, such as MYC targets and oxidative phosphorylation. Notably, the infection alters the cell surface by upregulating natural killer (NK)-activating ligands while simultaneously downregulating MHC class I molecules. Consequently, malignant cells become far more susceptible to NK-mediated cytotoxicity. In patient-derived samples, the virus selectively targets malignant cells and immunosuppressive myeloid subsets while leaving healthy hematopoietic progenitors unharmed.
A major breakthrough in this research involves the oncolytic virotherapy for myeloma induced shift toward a pro-inflammatory state. The virus promotes the activation of CD8+ T cells and drives monocytes toward an M1-like polarization. This immune remodeling triggers an inflammatory cytokine storm characterized by high levels of type I and II interferons. Furthermore, BoHV-1 upregulates CD38 expression on both myeloma and immune effector cells. This specific change significantly enhances the sensitivity of tumor cells to the monoclonal antibody daratumumab, offering a potent synergistic effect.
Combining BoHV-1 with established therapies like bortezomib or lenalidomide further increases anti-myeloma cytotoxicity. These findings suggest that BoHV-1 is not just an experimental tool but a versatile therapeutic agent. By coupling direct oncolysis with broad immune microenvironment remodeling, it addresses the core causes of treatment failure. Future clinical trials will likely explore these combination strategies to improve long-term outcomes for patients with refractory disease.
Unlike many human-derived viruses, BoHV-1 is nonpathogenic to humans. This means patients are unlikely to have pre-existing antiviral immunity that would neutralize the virus before it reaches the tumor site.
Yes, research shows that BoHV-1 works synergistically with bortezomib, lenalidomide, and daratumumab, potentially increasing the effectiveness of these standard treatments.
Monocytes are crucial for the virus's success. BoHV-1 shifts them from an immunosuppressive state to a pro-inflammatory (M1-like) state, which helps the immune system actively attack the cancer.
Disclaimer: This content is for informational and educational purposes only and does not constitute medical advice or a professional recommendation. Always consult a qualified healthcare provider for diagnosis and treatment. Refer to the latest local and national guidelines for clinical practice.
References
Raimondi V et al. Oncolytic bovine herpesvirus type 1 induces immune microenvironment remodeling and enhances treatment responses in multiple myeloma. Haematologica. 2026 Mar 26. doi: 10.3324/haematol.2025.289317. PMID: 41885031.
Raimondi V, Vescovini R, Dessena M, Donofrio G, Storti P, Giuliani N. Oncolytic viruses: a potential breakthrough immunotherapy for multiple myeloma patients. Front Immunol. 2024 Oct 30;15:1483806. doi: 10.3389/fimmu.2024.1483806.
Thorne SH. Potential of oncolytic viruses in the treatment of multiple myeloma. Mol Ther. 2016;24(6):1021-1022. doi:10.1038/mt.2016.66.
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