Abstract

Viral oncolysis, an approach to cancer therapy that emerged in the XX century and based on the natural ability of viruses to kill (lyse) cells in which it multiplies, has been developed in recent years by identifying viruses or their engineering variants with selective tumor replication. Over the past decades, a number of specific interactions of oncolytic viruses (both RNA and IDNA-containing) with malignant tumor cells have been described, individual candidate viruses and the types of tumors that they lase have been detected. The therapeutic efficacy of oncolytic viruses is achieved through a combination of selective destruction of tumor cells through a direct cytotoxic effect and activation of antitumor immunity; In addition, oncolytic viruses can affect abberant signaling pathways followed by blockade of tumor cell apoptosis, which gives the virus more time to complete its life cycle. A number of oncolytic viruses have shown promising therapeutic efficacy in preclinical studies in breast cancer; thus, the herpes simplex virus has a high selectivity for replication in tumor cells, which contributes to the death and the formation of infiltration of CD8+ and CD4+ T cells around tumor islands. The ability of reoviruses to enhance the expression of PD-L1 protein in cells was found, and the measles virus armed with the BNiP3 proapoptosis gene is more active in the cell lines of triple negative breast cancer. Improved viruses, from the point of view of the effectiveness and selectivity of effects on the tumor, as well as optimized combinations with other "standard" types of systemic therapy, are very promising, especially in patients with developed drug resistance.

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