Неврологические нарушения
May. 27th, 2021 06:38 pm![[personal profile]](https://www.dreamwidth.org/img/silk/identity/user.png){kind=small}
chuka_lisШведы обнаружили, что коронавирус в мозгу поражает перициты.
Неврологические симптомы были у тех больных ковидом, у кого были высокие и средние количества рецепторов АСЕ2 (с которыми соединяется коронавирус) на перицитах сосудов головного мозга. Вирусные частицы были обнаружены в клетках стенок сосудов, и в тех же местах были околососудистые воспаления в тканях с привлечением Т лимфоцитов и макрофагов, протечки фибриногена и нарушения гематоэнцефалического барьера. Маркеры в спинномозовой жидкости (PDGFRβ) так же показали, что в перицитах больных ковидом есть повреждения.
Here, we used state-of-the-art multiplexed immunostaining of human brains (n = 6 COVID-19, median age = 69,5 years; and n = 7 control, median age = 68 years), and demonstrated that expression of the SARS-CoV-2 receptor ACE2 is restricted to a subset of neurovascular pericytes. Strikingly, neurological symptoms were exclusive to, and ubiquitous in, patients that exhibited moderate to high ACE2 expression in peri-vascular cells. Viral particles were identified in the vascular wall and paralleled by peri-vascular inflammation, as signified by T cell and macrophage infiltration. Furthermore, fibrinogen leakage indicated compromised integrity of the blood-brain barrier. Notably, cerebrospinal fluid from an additional 16 individuals (n = 8 COVID-19, median age = 67 years; and n = 8 control, median age = 69,5 years) exhibited significantly lower levels of the pericyte marker PDGFRβ in SARS-CoV-2-infected cases, indicative of disrupted pericyte homeostasis.We conclude that pericyte infection by SARS-CoV-2 underlies virus entry into the privileged central nervous system space, as well as neurological symptomatology due to peri-vascular inflammation and a locally compromised blood-brain barrier.
Неврологические симптомы были у тех больных ковидом, у кого были высокие и средние количества рецепторов АСЕ2 (с которыми соединяется коронавирус) на перицитах сосудов головного мозга. Вирусные частицы были обнаружены в клетках стенок сосудов, и в тех же местах были околососудистые воспаления в тканях с привлечением Т лимфоцитов и макрофагов, протечки фибриногена и нарушения гематоэнцефалического барьера. Маркеры в спинномозовой жидкости (PDGFRβ) так же показали, что в перицитах больных ковидом есть повреждения.
Here, we used state-of-the-art multiplexed immunostaining of human brains (n = 6 COVID-19, median age = 69,5 years; and n = 7 control, median age = 68 years), and demonstrated that expression of the SARS-CoV-2 receptor ACE2 is restricted to a subset of neurovascular pericytes. Strikingly, neurological symptoms were exclusive to, and ubiquitous in, patients that exhibited moderate to high ACE2 expression in peri-vascular cells. Viral particles were identified in the vascular wall and paralleled by peri-vascular inflammation, as signified by T cell and macrophage infiltration. Furthermore, fibrinogen leakage indicated compromised integrity of the blood-brain barrier. Notably, cerebrospinal fluid from an additional 16 individuals (n = 8 COVID-19, median age = 67 years; and n = 8 control, median age = 69,5 years) exhibited significantly lower levels of the pericyte marker PDGFRβ in SARS-CoV-2-infected cases, indicative of disrupted pericyte homeostasis.We conclude that pericyte infection by SARS-CoV-2 underlies virus entry into the privileged central nervous system space, as well as neurological symptomatology due to peri-vascular inflammation and a locally compromised blood-brain barrier.
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