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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="other" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Problems of Virology</journal-id><journal-title-group><journal-title xml:lang="en">Problems of Virology</journal-title><trans-title-group xml:lang="ru"><trans-title>Вопросы вирусологии</trans-title></trans-title-group></journal-title-group><issn publication-format="print">0507-4088</issn><issn publication-format="electronic">2411-2097</issn><publisher><publisher-name xml:lang="en">Central Research Institute for Epidemiology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">11879</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Articles</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Статьи</subject></subj-group><subj-group subj-group-type="article-type"><subject></subject></subj-group></article-categories><title-group><article-title xml:lang="en">Role of cellular proteins in the life cycle of human immunodeficiency virus</article-title><trans-title-group xml:lang="ru"><trans-title>Роль клеточных белков в жизненном цикле вируса иммунодефицита</trans-title></trans-title-group></title-group><pub-date date-type="pub" iso-8601-date="2009-02-15" publication-format="electronic"><day>15</day><month>02</month><year>2009</year></pub-date><volume>54</volume><issue>1</issue><issue-title xml:lang="en">NO1 (2009)</issue-title><issue-title xml:lang="ru">№1 (2009)</issue-title><history><date date-type="received" iso-8601-date="2023-06-09"><day>09</day><month>06</month><year>2023</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2009, Bukrinskaya A.G., Bukrinskaya A.G.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2009, Букринская А.Г., Bukrinskaya A.G.</copyright-statement><copyright-year>2009</copyright-year><copyright-holder xml:lang="en">Bukrinskaya A.G., Bukrinskaya A.G.</copyright-holder><copyright-holder xml:lang="ru">Букринская А.Г., Bukrinskaya A.G.</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://virusjour.crie.ru/jour/article/view/11879">https://virusjour.crie.ru/jour/article/view/11879</self-uri><abstract xml:lang="en"><p>The paper shows a role of cellular proteins that control the early and late stages of HIV infection due to the keen genetic parasitism of human immunodeficiency virus (HIV). In its early life cycle, the virus uses the cell receptors CD4, CCR5, G-protein processor, and actin filaments of the cytoskeleton for nuclear transport. The cellular proteins transport the preintegration complex through the nuclear pores and assist complementary DNA to integrate with cellular DNA. At late stages, the cellular proteins provide the transport of viral components to the assemblage site - lipid rafts, the strong binding to them, the insertion of glycoproteins into the viral particle, and the cellular escape of the virus. To inhibit the cellular mechanisms involved in the infectious process is a new antiviral strategy approach to treating AIDS.</p></abstract><trans-abstract xml:lang="ru"><p>Показана роль клеточных белков, которые в результате изощренного генетического паразитизма вируса иммунодефицита человека (ВИЧ) регулируют ранние и поздние стадии ВИЧ-инфекции. На ранних стадиях жизненного цикла вирус использует клеточные рецепторы CD4, CCR5 и G-белок-процессор, актиновые волокна цитоскелета для транспорта в ядро. Клеточные белки осуществляют транспорт прединтеграционного комплекса через ядерные поры и помогают комплементарной ДНК интегрировать с клеточными ДНК. На поздних стадиях клеточные белки обеспечивают транспорт вирусных компонентов к месту сборки - липидным рафтам, прочное связывание с ними, встраивание гликопротеидов в вирусную частицу и выход вируса из клетки. Новым подходом антивирусной стратегии к лечению СПИДа является ингибирование клеточных механизмов, вовлеченных в инфекционный процесс.</p></trans-abstract><kwd-group xml:lang="en"><kwd>TIP47</kwd><kwd>human immunodeficiency virus</kwd><kwd>genetic parasitism</kwd><kwd>Gag progenitor</kwd><kwd>matrix protein</kwd><kwd>intracellular proteins</kwd><kwd>actin</kwd><kwd>inositol diphosphate</kwd><kwd>TIP47</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>вирус иммунодефицита человека</kwd><kwd>генетический паразитизм</kwd><kwd>Gag-предшественник</kwd><kwd>матриксный белок</kwd><kwd>внутриклеточный транспорт</kwd><kwd>клеточные белки</kwd><kwd>актин</kwd><kwd>инозитолдифосфат</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Букринская А. Г., Букринский М. И. 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