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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Acta Naturae</journal-id><journal-title-group><journal-title xml:lang="en">Acta Naturae</journal-title><trans-title-group xml:lang="ru"><trans-title>Acta Naturae</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2075-8251</issn><publisher><publisher-name xml:lang="en">Acta Naturae Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">10477</article-id><article-id pub-id-type="doi">10.32607/20758251-2015-7-2-6-16</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Reviews</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Обзоры</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Mechanisms of Oncolysis by Paramyxovirus Sendai</article-title><trans-title-group xml:lang="ru"><trans-title>Механизмы онколитического действия парамиксовируса Сендай</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Matveeva</surname><given-names>O. V.</given-names></name><name xml:lang="ru"><surname>Матвеева</surname><given-names>O. В.</given-names></name></name-alternatives><address><country country="US">United States</country></address><email>olga.matveeva@gmail.com</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Kochneva</surname><given-names>G. V.</given-names></name><name xml:lang="ru"><surname>Кочнева</surname><given-names>Г. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>olga.matveeva@gmail.com</email><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Netesov</surname><given-names>S. V.</given-names></name><name xml:lang="ru"><surname>Нетесов</surname><given-names>С. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>olga.matveeva@gmail.com</email><xref ref-type="aff" rid="aff3"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Onikienko</surname><given-names>S. B.</given-names></name><name xml:lang="ru"><surname>Оникиенко</surname><given-names>С. Б.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>olga.matveeva@gmail.com</email><xref ref-type="aff" rid="aff4"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Chumakov</surname><given-names>P. M.</given-names></name><name xml:lang="ru"><surname>Чумаков</surname><given-names>П. M</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>olga.matveeva@gmail.com</email><xref ref-type="aff" rid="aff5"/></contrib></contrib-group><aff id="aff1"><institution>Biopolymer Design</institution></aff><aff-alternatives id="aff2"><aff><institution xml:lang="en">Center of Virology and Biotechnology “Vector”</institution></aff><aff><institution xml:lang="ru">Государственный научный центр вирусологии и биотехнологии «Вектор»</institution></aff></aff-alternatives><aff-alternatives id="aff3"><aff><institution xml:lang="en">Novosibirsk State University</institution></aff><aff><institution xml:lang="ru">Новосибирский государственный университет</institution></aff></aff-alternatives><aff-alternatives id="aff4"><aff><institution xml:lang="en">Kirov Military Medical Academy</institution></aff><aff><institution xml:lang="ru">Военно-медицинская академия им. С.М. Кирова</institution></aff></aff-alternatives><aff-alternatives id="aff5"><aff><institution xml:lang="en">Engelhardt Institute of Molecular Biology</institution></aff><aff><institution xml:lang="ru">Институт молекулярной биологии им. В.А. Энгельгардта РАН</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2015-06-15" publication-format="electronic"><day>15</day><month>06</month><year>2015</year></pub-date><volume>7</volume><issue>2</issue><issue-title xml:lang="en">VOL 7, NO2 (2015)</issue-title><issue-title xml:lang="ru">ТОМ 7, №2 (2015)</issue-title><fpage>6</fpage><lpage>16</lpage><history><date date-type="received" iso-8601-date="2020-01-17"><day>17</day><month>01</month><year>2020</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2015, Matveeva O.V., Kochneva G.V., Netesov S.V., Onikienko S.B., Chumakov P.M.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2015, Матвеева O.В., Кочнева Г.В., Нетесов С.В., Оникиенко С.Б., Чумаков П.M.</copyright-statement><copyright-year>2015</copyright-year><copyright-holder xml:lang="en">Matveeva O.V., Kochneva G.V., Netesov S.V., Onikienko S.B., Chumakov P.M.</copyright-holder><copyright-holder xml:lang="ru">Матвеева O.В., Кочнева Г.В., Нетесов С.В., Оникиенко С.Б., Чумаков П.M.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://actanaturae.ru/2075-8251/article/view/10477">https://actanaturae.ru/2075-8251/article/view/10477</self-uri><abstract xml:lang="en"><p>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.</p></abstract><trans-abstract xml:lang="ru"><p>Некоторые представители парамиксовирусов обладают онколитической активностью и могут использоваться в качестве противоопухолевых агентов. Такие парамиксовирусы включают непатогенные (аттенуированные) штаммы вирусов кори, вируса болезни Ньюкасла и вируса Сендай. Все эти вирусы и вирус Сендай, в частности, способны вызывать в большой степени специфическую гибель именно злокачественных, но не нормальных клеток. Гибель злокачественных клеток происходит за счет прямого цитолитического действия вируса, а также как следствие активации противоопухолевого иммунитета. Преимущественное взаимодействие парамиксовирусов со злокачественными клетками происходит за счет того, что эти клетки в избытке продуцируют некоторые гликопротеины, способные служить рецепторами для онколитических парамиксовирусов. Кроме того, частые генетические дефекты раковых клеток в системе интерферонового и апоптозного ответов создают благоприятные условия для репликации вируса именно в злокачественных клетках. Парамиксовирусы могут усиливать образование многоядерных клеточных конгломератов (синцитиев), что ускоряет вовлечение новых клеток в инфекционный процесс внутри опухоли и позволяет вирусу ускользать от нейтрализующего воздействия антител. Все эти факторы способствуют эффективному внутриопухолевому распространению вирусной инфекции и массовой гибели злокачественных клеток. Кроме того, онколитические парамиксовирусы способны вызывать иммуноопосредованную гибель злокачественных клеток. Они действуют как мощные индукторы интерферона и других цитокинов, стимулирующих противоопухолевую активность различных клеточных компонентов иммунного ответа, таких, как дендритные клетки, натуральные киллеры и цитотоксические Т-лимфоциты. Обнадеживающие результаты, полученные в различных исследованиях, проводимых с онколитическими парамиксовирусами, можно объяснить действием указанных механизмов.</p></trans-abstract><kwd-group xml:lang="en"><kwd>attenuated measles virus strains</kwd><kwd>Newcastle disease virus</kwd><kwd>Sendai virus</kwd><kwd>oncolytic paramyxoviruses</kwd><kwd>viral anti-tumor mechanism</kwd><kwd>viral anticancer immune stimulation</kwd><kwd>cancer therapy</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>вакцинные штаммы вируса кори</kwd><kwd>вирус болезни Ньюкасла</kwd><kwd>вирус Сендай</kwd><kwd>онколитические парамиксовирусы</kwd><kwd>противоопухолевый механизм</kwd><kwd>противоопухолевый иммунитет</kwd><kwd>терапия рака</kwd></kwd-group><funding-group><funding-statement xml:lang="en">This work was supported by a grant from the Ministry of Education and Science (RFMEFI60714X0014), as well as from the Russian Science Foundation (grant No. 14-15-01073).</funding-statement><funding-statement xml:lang="ru">Работа поддержана грантом Министерства образования и науки (RFMEFI60714X0014), а также РНФ (грант № 14-15-01073).</funding-statement></funding-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>[1] Svejda J. // Lek. 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