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description Publicationkeyboard_double_arrow_right Article , Other literature type 2023 France EnglishPublisher:Free Neuropathology Funded by:ANR | NeurATRIS, WTANR| NeurATRIS ,WTBoluda, Susana; Mokhtari, Karima; Mégarbane, Bruno; Annane, Djillali; Mathon, Bertrand; Cao, Albert; Adam, Clovis; Androuin, Alexandre; Bielle, Franck; Brochier, Guy; Charlotte, Frédéric; Chougar, Lydia; Khalid, Hamid; Eloit, Marc; Haïk, Stéphane; Hervé, Dominique; Kasri, Amal; Leducq, Valentin; Lehéricy, Stéphane; Levavasseur, Etienne; Lobsiger, Christian; Lorin La Grandmaison, Geoffroy; Malet, Isabelle; Malissin, Isabelle; Marot, Stéphane; Marty, Serge; Pérot, Philippe; Plu, Isabelle; Prigent, Annick; Stimmer, Lev; Potier, Marie-Claude; Marcelin, Anne-Geneviève; Delatour, Benoît; Duyckaerts, Charles; Seilhean, Danielle;In a neuropathological series of 20 COVID-19 cases, we analyzed six cases (three biopsies and three autopsies) with multiple foci predominantly affecting the white matter as shown by MRI. The cases presented with microhemorrhages evocative of small artery diseases. This COVID-19 associated cerebral microangiopathy (CCM) was characterized by perivascular changes: arterioles were surrounded by vacuolized tissue, clustered macrophages, large axonal swellings and a crown arrangement of aquaporin-4 immunoreactivity. There was evidence of blood-brain-barrier leakage. Fibrinoid necrosis, vascular occlusion, perivascular cuffing and demyelination were absent. While no viral particle or viral RNA was found in the brain, the SARS-CoV-2 spike protein was detected in the Golgi apparatus of brain endothelial cells where it closely associated with furin, a host protease known to play a key role in virus replication. Endothelial cells in culture were not permissive to SARS-CoV-2 replication. The distribution of the spike protein in brain endothelial cells differed from that observed in pneumocytes. In the latter, the diffuse cytoplasmic labeling suggested a complete replication cycle with viral release, notably through the lysosomal pathway. In contrast, in cerebral endothelial cells the excretion cycle was blocked in the Golgi apparatus. Interruption of the excretion cycle could explain the difficulty of SARS-CoV-2 to infect endothelial cells in vitro and to produce viral RNA in the brain. Specific metabolism of the virus in brain endothelial cells could weaken the cell walls and eventually lead to the characteristic lesions of COVID-19 associated cerebral microangiopathy. Furin as a modulator of vascular permeability could provide some clues for the control of late effects of microangiopathy. Free Neuropathology, Vol. 4 (2023)
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description Publicationkeyboard_double_arrow_right Article , Other literature type 2023 France EnglishPublisher:Free Neuropathology Funded by:ANR | NeurATRIS, WTANR| NeurATRIS ,WTBoluda, Susana; Mokhtari, Karima; Mégarbane, Bruno; Annane, Djillali; Mathon, Bertrand; Cao, Albert; Adam, Clovis; Androuin, Alexandre; Bielle, Franck; Brochier, Guy; Charlotte, Frédéric; Chougar, Lydia; Khalid, Hamid; Eloit, Marc; Haïk, Stéphane; Hervé, Dominique; Kasri, Amal; Leducq, Valentin; Lehéricy, Stéphane; Levavasseur, Etienne; Lobsiger, Christian; Lorin La Grandmaison, Geoffroy; Malet, Isabelle; Malissin, Isabelle; Marot, Stéphane; Marty, Serge; Pérot, Philippe; Plu, Isabelle; Prigent, Annick; Stimmer, Lev; Potier, Marie-Claude; Marcelin, Anne-Geneviève; Delatour, Benoît; Duyckaerts, Charles; Seilhean, Danielle;In a neuropathological series of 20 COVID-19 cases, we analyzed six cases (three biopsies and three autopsies) with multiple foci predominantly affecting the white matter as shown by MRI. The cases presented with microhemorrhages evocative of small artery diseases. This COVID-19 associated cerebral microangiopathy (CCM) was characterized by perivascular changes: arterioles were surrounded by vacuolized tissue, clustered macrophages, large axonal swellings and a crown arrangement of aquaporin-4 immunoreactivity. There was evidence of blood-brain-barrier leakage. Fibrinoid necrosis, vascular occlusion, perivascular cuffing and demyelination were absent. While no viral particle or viral RNA was found in the brain, the SARS-CoV-2 spike protein was detected in the Golgi apparatus of brain endothelial cells where it closely associated with furin, a host protease known to play a key role in virus replication. Endothelial cells in culture were not permissive to SARS-CoV-2 replication. The distribution of the spike protein in brain endothelial cells differed from that observed in pneumocytes. In the latter, the diffuse cytoplasmic labeling suggested a complete replication cycle with viral release, notably through the lysosomal pathway. In contrast, in cerebral endothelial cells the excretion cycle was blocked in the Golgi apparatus. Interruption of the excretion cycle could explain the difficulty of SARS-CoV-2 to infect endothelial cells in vitro and to produce viral RNA in the brain. Specific metabolism of the virus in brain endothelial cells could weaken the cell walls and eventually lead to the characteristic lesions of COVID-19 associated cerebral microangiopathy. Furin as a modulator of vascular permeability could provide some clues for the control of late effects of microangiopathy. Free Neuropathology, Vol. 4 (2023)
Europe PubMed Centra... arrow_drop_down HAL-Pasteur; Mémoires en Sciences de l'Information et de la Communication; HAL-CEAArticle . 2023License: CC BYadd ClaimPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
You have already added works in your ORCID record related to the merged Research product.This Research product is the result of merged Research products in OpenAIRE.
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For further information contact us at helpdesk@openaire.euAccess RoutesGreen 0 citations 0 popularity Average influence Average impulse Average Powered by BIP!more_vert Europe PubMed Centra... arrow_drop_down HAL-Pasteur; Mémoires en Sciences de l'Information et de la Communication; HAL-CEAArticle . 2023License: CC BYadd ClaimPlease grant OpenAIRE to access and update your ORCID works.This Research product is the result of merged Research products in OpenAIRE.
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