Продолжающаяся пандемия коронавирусной болезни – 2019 (COVID-19) диктует необходимость изучения молекулярных и клеточных механизмов взаимодействия возбудителя и организма человека. Проявление неврологических симптомов у некоторых пациентов с COVID-19 представляет проблему для нейробиологов в виду недостаточно изученного патоморфогенеза заболевания. В настоящем обзоре систематизированы литературные данные, отражающие пути проникновения SARS-CoV-2 в головной мозг, особенности его взаимодействия с нейронами, нейроглией и иммунными клетками. Показано, что основными механизмами нейроинвазии SARS-CoV-2 предположительно являются ретроградный аксональный транспорт по волокнам обонятельного и блуждающего нервов; проникновение через поврежденный гематоэнцефалический барьер (ГЭБ) или миграция иммунокомпетентных клеток, содержащих вирусные частицы, через неповрежденный ГЭБ. Установлено, что вирус-индуцибельная гибель нейронов обусловлена не только прямым цитотоксическим эффектом, но также обусловлена дисрегуляцией ренинангиотензиновой системы мозга и высвобождением большого количества воспалительных цитокинов как проявлением «цитокинового шторма». Продемонстрировано участие клеток нейроглии в инициации и поддержании нейровоспалительных и нейродегенеративных процессов вследствие активации их провоспалительного фенотипа. Обсуждается роль тучных клеток вмеханизмах противовирусной защиты и воспалительных реакциях.
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