Mechanisms of Oncolysis by Paramyxovirus Sendai
- Authors: Matveeva O.V.1, Kochneva G.V.2, Netesov S.V.3, Onikienko S.B.4, Chumakov P.M.5
-
Affiliations:
- Biopolymer Design
- Center of Virology and Biotechnology “Vector”
- Novosibirsk State University
- Kirov Military Medical Academy
- Engelhardt Institute of Molecular Biology
- Issue: Vol 7, No 2 (2015)
- Pages: 6-16
- Section: Reviews
- Submitted: 17.01.2020
- Published: 15.06.2015
- URL: https://actanaturae.ru/2075-8251/article/view/10477
- DOI: https://doi.org/10.32607/20758251-2015-7-2-6-16
- ID: 10477
Cite item
Abstract
Some viral strains of the Paramyxoviridae family may be used as anti-tumor agents. Oncolytic paramyxoviruses include attenuated strains of the measles virus, Newcastle disease virus, and Sendai virus. These viral strains, and the Sendai virus in particular, can preferentially induce the death of malignant, rather than normal, cells. The death of cancer cells results from both direct killing by the virus and through virus-induced activation of anticancer immunity. Sialic-acid-containing glycoproteins that are overexpressed in cancer cells serve as receptors for some oncolytic paramyxoviruses and ensure preferential interaction of paramyxoviruses with malignant cells. Frequent genetic defects in interferon and apoptotic response systems that are common to cancer cells ensure better susceptibility of malignant cells to viruses. The Sendai virus as a Paramyxovirus is capable of inducing the formation of syncytia, multinuclear cell structures which promote viral infection spread within a tumor without virus exposure to host neutralizing antibodies. As a result, the Sendai virus can cause mass killing of malignant cells and tumor destruction. Oncolytic paramyxoviruses can also promote the immune-mediated elimination of malignant cells. In particular, they are powerful inducers of interferon and other cytokynes promoting antitumor activity of various cell components of the immune response, such as dendritic and natural killer cells, as well as cytotoxic T lymphocytes. Taken together these mechanisms explain the impressive oncolytic activity of paramyxoviruses that hold promise as future, efficient anticancer therapeutics.
About the authors
O. V. Matveeva
Biopolymer Design
Author for correspondence.
Email: olga.matveeva@gmail.com
United States
G. V. Kochneva
Center of Virology and Biotechnology “Vector”
Email: olga.matveeva@gmail.com
Russian Federation
S. V. Netesov
Novosibirsk State University
Email: olga.matveeva@gmail.com
Russian Federation
S. B. Onikienko
Kirov Military Medical Academy
Email: olga.matveeva@gmail.com
Russian Federation
P. M. Chumakov
Engelhardt Institute of Molecular Biology
Email: olga.matveeva@gmail.com
Russian Federation
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