Тромбоциты при COVID-19: «случайные прохожие» или соучастники?

Одной из наиболее опасных особенностей новой коронавирусной инфекции, вызванной вирусом SARS-CoV-2, является склонность системы гемостаза больных к избыточному тромбообразованию. Среди возможных причин данной патологии выделяют как активацию эндотелиоцитов сосудов, приводящую к выставлению тканевого фактора этими клетками, так и активацию плазменного звена гемостаза. Кроме того, показано, что при SARS-CoV-2 наблюдается значительное изменение функциональных ответов тромбоцитов на активацию, которое, однако, не сопровождается значительной тромбоцитопенией. Механизм влияния на функциональность и количество тромбоцитов представляется достаточно противоречивым. С одной стороны, существуют предположения, что тромбоциты могут выступать непосредственным «контейнером» для вируса, распространяя по организму. С другой стороны, наличие вирусной РНК в тромбоцитах было продемонстрировано только в одном исследовании, тогда как другие авторы получили обратный результат. Еще одним механизмом непосредственного воздействия вируса на тромбоциты является его проникновение в мегакариоциты и последующее нарушение тромбоцитопоэза. Тем не менее в 3 из 4 опубликованных на настоящий момент работ показано, что тромбоциты пациентов с SARS-CoV-2 находятся в активированном состоянии (так называемая подактивация тромбоцитов). Это явление может быть вызвано как прямым влиянием вируса, так и влиянием на функции тромбоцитов идущего в легких процесса. В настоящем обзоре мы рассматриваем существующие данные и возможные причины изменения функциональности тромбоцитов, наблюдаемого у пациентов с SARS-CoV-2. 

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