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  • Evaluation of Newcastle Disease Virus-Induced Natural Killer Cell Activation and Its Potential Antitumor Effects

  • Maryam.Anari,1 Abolfaz.Barzegari,2,* Parisa.Gozali,3 Parasto.Mirzaei,4
    1. Department of Medical Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
    2. Department of Medical Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
    3. Department of Molecular Medicine, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
    4. Department of Medical Nanotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran


  • Introduction: Natural killer (NK) cells are a prominent population of innate lymphoid cells (ILCs) that contribute critically to antigen-independent immune surveillance against tumor cells and virally infected cells. As opposed to cells of the adaptive immune lineage, which depend on somatic gene rearrangements to generate antigen-specific receptor molecules, NK cell activation is regulated by the integration of multiple signals from germline-encoded stimulatory and suppressive cell-surface receptors. Activated NK cells carry out cell-contact-dependent cytotoxicity through the targeted exocytosis of lytic granules containing perforin and granzyme B. They also induce death receptor-mediated apoptosis signaling pathways, such as the FASL and TRAIL pathways, in target cells. Concurrently, NK cells release inflammation-promoting cytokines, particularly interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α), which are essential for stimulating antigen-presenting cells (APCs) and mediating subsequent adaptive Th1-polarized immunological responses. Oncolytic Newcastle Disease Virus (NDV), an enveloped, negative-sense, single-stranded RNA paramyxovirus, selectively replicates in and lyses cancer cells due to disrupted antiviral type I interferon (IFN) signaling.. The ability of viruses to stimulate NK cells points to principal mechanisms that drive this inflammatory remodeling in the tumor microenvironment.
  • Methods: In this study, we obtained the outcomes of associated articles published between 2020 and 2026 using keywords such as "Newcastle disease virus" AND "NK cell" AND (activation OR cytotoxicity) AND (antitumor OR "anti-tumor" OR oncolytic) -meta-analysis -systematic queries from reputable databases. Information from these articles was retrieved and interpreted in this review.
  • Results: Recent studies illustrated the pivotal role of Newcastle disease virus (NDV)-induced immunopotentiation and combination strategies in natural killer (NK) cell activation and targeted tumor regression. These studies reported that viral structures and immunotherapeutic adjuvants, for example, interferon-mediated regulation of the PD-L1/MICA axis (1), the pan-protein tyrosine phosphatase inhibitor vanadyl sulfate (2), HN-Fc-CD16 and HN-Fc-IL-15-CD16 bi/tri-specific antibodies (3), the viral hemagglutinin-neuraminidase (HN) glycoprotein binding to natural cytotoxicity receptors (4), virus-induced inflammatory cytokines triggering NK tumor infiltration (5), recombinant GM-CSF-expressing NDV variants like MEDI5395 (6), metabolic glycolysis inhibitors such as dichloroacetate(7), and non-lytic viral strains like NDV Ulster (8) are capable to impact the molecular pathways, accordingly can induce stirring receptor signaling, the release of perforin and granzyme B, interferon-gamma (IFN-γ) secretion, and substantial lytic and non-lytic antitumor activity in diverse malignant cells.
  • Conclusion: These articles indicated that oncolytic NDV significantly stimulates natural killer (NK) cells by reducing the immunosuppressive PD-L1/MICA balance and triggering activating cytotoxicity receptors. Combining NDV with synergistic therapeutic agents—including the glycolysis inhibitor dichloroacetate (DCA), vanadyl sulfate, recombinant MEDI5395, or HN-engaging bi/tri-specific antibodies—synergistically drives robust IFN-γ secretion, granzyme B release, and potent antitumor cytotoxicity to eliminate refractory malignant tumors.
  • Keywords: Natural Killer Cells (NK Cells), NK Cell Activation, Antitumor Immunity, Oncolytic Virotherapy

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