Клеточные и надклеточные уровни взаимодействия ретровирусов с хозяином на примере вируса бычьего лейкоза. Сообщение II. Критические стадии - поливариантность, универсальность (обзор)

Автор: Глазко В.И., Косовский Г.Ю., Федорова Л.М., Глазко Т.Т.

Журнал: Сельскохозяйственная биология @agrobiology

Рубрика: Обзоры, проблемы

Статья в выпуске: 6 т.56, 2021 года.

Бесплатный доступ

Широкое распространение вирусных инфекций, легкость преодоления видовых барьеров вирус-специфичности требуют определить критические стадии в процессах взаимодействия вирусов с многоклеточными организмами млекопитающих и ключевые молекулярно-генетические системы для каждой из стадий. К настоящему времени уже накоплено большое количество данных о разнообразии и сложности таких систем, а также вовлеченности в них широкого спектра метаболических путей. В этой связи особую актуальность приобретает выявление в них некоторых элементов, общих для разных инфекционных процессов. Настоящий обзор предлагает такой подход на примере анализа основных событий при инфицировании крупного рогатого скота вирусом бычьего лейкоза (BLV). В соответствии с критическими стадиями выделены системы, участвующие в проникновении генетического материала BLV в цитоплазму клеток хозяина, угнетении врожденного и адаптивного иммунитета, а также во взаимодействии между геномами провируса BLV и геномом хозяина. В трансмембранных системах хозяина присутствуют непосредственные участники рецепции вирусных белков (G.Yu. Kosovskii с соавт., 2017; V.I. Glazko с соавт., 2018; L. Bai с соавт., 2019; H. Sato с соавт., 2020) и факторы, модифицирующие оболочечные белки вирусов при их размножении в клетках хозяина (A. De Brogniez с соавт., 2016; W. Assi с соавт., 2020). Как и в случае оболочечных белков BLV, у SARS-CoV-2 (COVID-19) модификации белков шипа оказывают существенное влияние на патогенность (M. Hoffmann с соавт., 2020). Патогенность и BLV, и COVID-19 во многом определяется их угнетающим действием на врожденный и адаптивный иммунитет, в частности через активацию Т-регуляторных клеток и повышение экспрессии рост-трансформирующего фактора TGF-b (L.Y. Chang с соавт., 2015; G.Yu. Kosovskii с соавт., 2017; W. Chen с соавт., 2020). Внутриклеточные механизмы защиты от ретротранспозиций, рекомбинаций между вирусами и ретротранспозонами хозяина, формирования новых элементов регуляторных сетей хозяина типа микроРНК, интеграции провирусной ДНК в геном хозяина тесно связаны и контролируются системами интерферирующей РНК (RNAi) с участием их ключевого гена dicer1 (P.V. Maillard с соавт., 2019; E.Z. Poirier с соавт., 2021; G.Y. Kosovsky с соавт., 2020). Можно ожидать, что именно эти системы обеспечивают определенную устойчивость генома к встраиванию в него экзогенного генетического материала и ограничение активных транспозиций собственных мобильных генетических элементов. По-видимому, именно полигенность контроля перечисленных критических стадий вирусных инфекций приводит к сложностям прогноза и предупреждения их развития.

Еще

Вирус бычьего лейкоза, blv, sars-cov-2, hiv-1, трансмембранные системы, врожденный и адаптивный иммунитет, системы интерферирующей рнк, транспозиции, мобильные генетические элементы

Короткий адрес: https://sciup.org/142231901

IDR: 142231901   |   DOI: 10.15389/agrobiology.2021.6.1079rus

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