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1.
Eur Rev Med Pharmacol Sci ; 25(15): 5063-5069, 2021 08.
Article in English | MEDLINE | ID: covidwho-1346861

ABSTRACT

OBJECTIVE: Vaccine-induced immune thrombocytopenia (VITT) is a new syndrome occurring primarily in healthy young adults, with a female predominance, after receiving the first dose of ChAdOx1 nCoV-19 vaccine. We describe VITT syndrome characterized by severe thrombosis and thrombocytopenia found in our patient, with fatal outcome. CASE REPORT: A 58-year-old man, after 13 days from the first administration of ChAdOx1 nCoV-19 vaccine (AstraZeneca), presented with abdominal pain, diarrhea and vomitus. Laboratory tests revealed a severe thrombocytopenia, low fibrinogen serum levels and marked increase of D-dimer serum levels. The patient quickly developed a multiple organ failure, till death, three days after the hospital admission. RESULTS: At histology, in the lungs, interalveolar septa appeared thickened with microthrombi in the capillaries and veins. Interalveolar septa appeared thickened and showed vascular proliferation. Thrombi were detected in the capillaries of glomerular tufts. In the hearth, thrombi were observed in veins and capillaries. In the liver, voluminous fibrin thrombi were diffusely observed in the branches of the portal vein. Microthrombi were also found in the vasa vasorum of the wall of abdominal aorta. In the brain, microthrombi were observed in the capillaries of the choroid plexuses. Diffuse hemorrhagic necrosis was observed in the intestinal wall with marked congestion of the venous vessels. CONCLUSIONS: In our patient, the majority of data necessary for a VITT final diagnosis were present: thrombocytopenia and thrombosis in pulmonary, portal, hepatic, renal and mesenteric veins, associated with a marked increase of D-dimer serum levels. The finding of cerebral thrombosis in choroid plexuses, is a new finding in VITT. These features are suggestive for a very aggressive form of VITT.


Subject(s)
COVID-19 Vaccines/adverse effects , COVID-19/prevention & control , Purpura, Thrombocytopenic, Idiopathic/etiology , Thrombosis/etiology , Aorta/pathology , COVID-19/blood , COVID-19 Vaccines/administration & dosage , Choroid Plexus/pathology , Fibrin Fibrinogen Degradation Products/metabolism , Humans , Ileum/pathology , Kidney/pathology , Liver/pathology , Lung/pathology , Male , Middle Aged , Myocardium/pathology , Purpura, Thrombocytopenic, Idiopathic/blood , Thrombosis/blood
2.
Nature ; 595(7868): 565-571, 2021 07.
Article in English | MEDLINE | ID: covidwho-1275939

ABSTRACT

Although SARS-CoV-2 primarily targets the respiratory system, patients with and survivors of COVID-19 can suffer neurological symptoms1-3. However, an unbiased understanding of the cellular and molecular processes that are affected in the brains of patients with COVID-19 is missing. Here we profile 65,309 single-nucleus transcriptomes from 30 frontal cortex and choroid plexus samples across 14 control individuals (including 1 patient with terminal influenza) and 8 patients with COVID-19. Although our systematic analysis yields no molecular traces of SARS-CoV-2 in the brain, we observe broad cellular perturbations indicating that barrier cells of the choroid plexus sense and relay peripheral inflammation into the brain and show that peripheral T cells infiltrate the parenchyma. We discover microglia and astrocyte subpopulations associated with COVID-19 that share features with pathological cell states that have previously been reported in human neurodegenerative disease4-6. Synaptic signalling of upper-layer excitatory neurons-which are evolutionarily expanded in humans7 and linked to cognitive function8-is preferentially affected in COVID-19. Across cell types, perturbations associated with COVID-19 overlap with those found in chronic brain disorders and reside in genetic variants associated with cognition, schizophrenia and depression. Our findings and public dataset provide a molecular framework to understand current observations of COVID-19-related neurological disease, and any such disease that may emerge at a later date.


Subject(s)
Astrocytes/pathology , Brain/pathology , COVID-19/diagnosis , COVID-19/pathology , Choroid Plexus/pathology , Microglia/pathology , Neurons/pathology , Aged , Aged, 80 and over , Brain/metabolism , Brain/physiopathology , Brain/virology , COVID-19/genetics , COVID-19/physiopathology , Cell Nucleus/genetics , Choroid Plexus/metabolism , Choroid Plexus/physiopathology , Choroid Plexus/virology , Female , Humans , Inflammation/virology , Male , Middle Aged , SARS-CoV-2/growth & development , SARS-CoV-2/pathogenicity , Single-Cell Analysis , Transcriptome , Virus Replication
3.
Stem Cell Reports ; 16(5): 1156-1164, 2021 05 11.
Article in English | MEDLINE | ID: covidwho-1225409

ABSTRACT

Coronavirus disease 2019 (COVID-19) patients have manifested a variety of neurological complications, and there is still much to reveal regarding the neurotropism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Human stem cell-derived brain organoids offer a valuable in vitro approach to study the cellular effects of SARS-CoV-2 on the brain. Here we used human embryonic stem cell-derived cortical organoids to investigate whether SARS-CoV-2 could infect brain tissue in vitro and found that cortical organoids could be infected at low viral titers and within 6 h. Importantly, we show that glial cells and cells of the choroid plexus were preferentially targeted in our model, but not neurons. Interestingly, we also found expression of angiotensin-converting enzyme 2 in SARS-CoV-2 infected cells; however, viral replication and cell death involving DNA fragmentation does not occur. We believe that our model is a tractable platform to study the cellular effects of SARS-CoV-2 infection in brain tissue.


Subject(s)
COVID-19/pathology , Choroid Plexus/pathology , Human Embryonic Stem Cells/cytology , Neuroglia/virology , Organoids/innervation , Organoids/pathology , Cells, Cultured , Choroid Plexus/cytology , Choroid Plexus/virology , Humans , Neuroglia/pathology , Neurons/virology , Organoids/cytology , SARS-CoV-2/pathogenicity
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