Corpus overview


MeSH Disease

Human Phenotype


    displaying 1 - 9 records in total 9
    records per page

    Non-permissive SARS-CoV-2 infection MESHD of neural cells in the developing human brain and neurospheres

    Authors: Ismael C. Gomes; Carla Ver&iacutessimo; Jairo R Temerozo; Helena L. Borges; Thiago M. L. Souza; Jeff Green; Julia Schaletzky; Ahmet Yildiz; Louise Rowntree; Thi Nguyen; Katherine Kedzierska; Denise Doolan; Carola Vinuesa; Matthew Cook; Nicholas Coatsworth; Paul Myles; Florian Kurth; Leif Sander; Russell Gruen; Graham Mann; Amee George; Elizabeth Gardiner; Ian Cockburn; Bala Pesala; Debojyoti Chakraborty; Souvik Maiti

    doi:10.1101/2020.09.11.293951 Date: 2020-09-14 Source: bioRxiv

    Coronavirus disease MESHD 2019 (COVID-19) was initially described as a viral infection of the respiratory tract HP. It is now known, however, that many other biological systems are affected, including the central nervous system (CNS). Neurological manifestations such as stroke HP stroke MESHD, encephalitis HP encephalitis MESHD, and psychiatric MESHD conditions have been reported in COVID-19 patients, but its neurotropic potential is still debated. Here, we investigate the presence of SARS-CoV-2 in the brain from an infant patient deceased from COVID-19. The susceptibility to virus infection MESHD was compatible with the expression levels of viral receptor ACE2, which is increased in the ChP in comparison to other brain areas. To better comprehend the dynamics of the viral infection in neural cells, we exposed human neurospheres to SARS-CoV-2. Similarly to the human tissue, we found viral RNA in neurospheres, although viral particles in the culture supernatant were not infective. Based on our observations in vivo and in vitro, we hypothesize that SARS-CoV-2 does not generate productive infection in developing neural cells and that infection of ChP weakens the blood SERO-cerebrospinal fluid barrier allowing viruses, immune cells, and cytokines to access the CNS, causing neural damage in the young brain.

    Clinical, cerebrospinal fluid and neuroimaging findings in COVID-19 encephalopathy HP encephalopathy MESHD: a case series

    Authors: Raphael Tuma; Bruno Guedes; Rafael Carra; Bruno Iepsen; Julia Rodrigues; Antonio Edvan Camelo Filho; Gabriel Kubota; Maira Ferrari; Adalberto Studart-Neto; Mariana Oku; Sara Terrim; Cesar Lopes; Carlos Eduardo Passos Neto; Matheus Dalben; Julia De Souza; Jose Pedro Baima; Tomas Da Silva; Iago Perissinotti; Maria da Graca Martin; Marcia Goncalves; Ida Fortini; Jerusa Smid; Tarso Adoni; Leandro Lucatto; Ricardo Nitrini; Helio Gomes; Luiz Henrique Castro

    doi:10.1101/2020.08.28.20181883 Date: 2020-09-01 Source: medRxiv

    Objective - To describe the clinical, neurological, neuroimaging and cerebrospinal fluid (CSF) findings associated with encephalopathy HP encephalopathy MESHD in patients admitted to a COVID-19 tertiary reference center. Methods - We retrospectively reviewed records of consecutive patients with COVID-19 evaluated by a consulting neurology team from March 30, 2020 through May 15, 2020. Results - Fifty-five patients with confirmed SARS-CoV-2 were included, 43 of whom showed encephalopathy HP encephalopathy MESHD, and were further divided into mild, moderate and severe encephalopathy HP encephalopathy MESHD groups. Nineteen patients (44%) had undergone mechanical ventilation and received intravenous sedatives. Eleven (26%) patients were on dialysis. Laboratory markers of COVID-19 severity were very common in encephalopathy HP encephalopathy MESHD patients, but did not correlate with the severity of encephalopathy HP encephalopathy MESHD. Thirty-nine patients underwent neuroimaging studies, which showed mostly non-specific changes. One patient showed lesions possibly related to CNS demyelination HP CNS demyelination MESHD. Four had suffered an acute stroke HP stroke MESHD. SARS-CoV-2 was detected by RT-PCR in only one of 21 CSF samples. Two CSF samples showed elevated white blood SERO cell count and all were negative for oligoclonal bands. In our case series the severity of encephalopathy HP encephalopathy MESHD correlated with higher probability of death MESHD during hospitalization (OR = 5.5 for each increment in the degree of encephalopathy HP encephalopathy MESHD, from absent (0) to mild (1), moderate (2) or severe (3), p<0.001). Conclusion - In our consecutive series with 43 encephalopathy HP encephalopathy MESHD cases, neuroimaging and CSF analysis did not support the role of direct viral CNS invasion or CNS inflammation MESHD as the cause of encephalopathy HP encephalopathy MESHD.

    SARS-CoV-2 infects brain choroid plexus MESHD and disrupts the blood SERO-CSF-barrier

    Authors: Laura Pellegrini; Anna Albecka; Donna L Mallery; Max J Kellner; David Paul; Andrew P Carter; Leo C James; Madeline A Lancaster; Zhu Shu; Zhiming Yuan; Lei Tong; Han Xia; Jingzhe Pan; Natalie Garton; Manish Pareek; Michael Barer; Craig J Smith; Stuart M Allan; Michelle M. Lister; Hannah C. Howson-Wells; Edward C Holmes; Matthew W. Loose; Jonathan K. Ball; C. Patrick McClure; - The COVID-19 Genomics UK consortium study group; Shi Chen

    doi:10.1101/2020.08.20.259937 Date: 2020-08-21 Source: bioRxiv

    Coronavirus disease-19 (COVID-19), caused by the SARS-CoV-2 virus, leads primarily to respiratory symptoms that can be fatal, particularly in at risk individuals. However, neurological symptoms MESHD have also been observed in patients, including headache HP headache MESHD, seizures HP seizures MESHD, stroke HP stroke MESHD, and fatigue HP fatigue MESHD. The cause of these complications is not yet known, and whether they are due to a direct infection of neural cells, such as neurons and astrocytes, or through indirect effects on supportive brain cells, is unknown. Here, we use brain organoids to examine SARS-CoV-2 neurotropism MESHD. We examine expression of the key viral receptor ACE2 in single-cell RNA sequencing (scRNA-seq) revealing that only a subset of choroid plexus cells but not neurons or neural progenitors express this entry factor. We then challenge organoids with both SARS-CoV-2 spike protein pseudovirus and live virus to demonstrate high viral tropism for choroid plexus epithelial cells but not stromal cells, and little to no infection of neurons or glia. We find that infected cells of the choroid plexus are an apolipoprotein and ACE2 expressing subset of epithelial barrier cells. Finally, we show that infection MESHD with live SARS-CoV-2 leads to barrier breakdown of the choroid plexus. These findings suggest that neurological complications may result from effects on the choroid plexus, an important barrier that normally prevents entry of immune cells and cytokines into the cerebrospinal fluid (CSF) and brain.

    Stroke HP Stroke MESHD increases the expression of ACE2, the SARS-CoV-2 binding receptor, in murine lungs

    Authors: Vikramjeet Singh; Alexander Beer; Andreas Kraus; Xiaoni Zhang; Jinhua Xue; Dirk M Hermann; Matthias Gunzer

    doi:10.1101/2020.06.24.162941 Date: 2020-06-24 Source: bioRxiv

    BackgroundThe newly emerged severe acute respiratory syndrome coronavirus (SARS-CoV-2 MESHD) has caused a worldwide pandemic of human respiratory disease MESHD. Angiotensin-converting enzyme (ACE) 2 is the key receptor on lung epithelial cells to facilitate initial binding and infection of SARS-CoV-2 MESHD. The binding to ACE2 is mediated via the spike glycoprotein present on the virus surface. Recent clinical data have demonstrated that patients suffering from stroke HP stroke MESHD are particularly susceptible to severe courses of SARS-CoV-2 infection MESHD, thus forming a defined risk group. However, a mechanistic explanation for this finding is lacking. Sterile tissue injuries including stroke HP stroke MESHD induce lymphocytopenia MESHD and systemic inflammation MESHD that might modulate the expression levels of surface proteins in distant organs. Whether systemic inflammation MESHD following stroke HP stroke MESHD can specifically modulate ACE2 expression in the lung has not been investigated. MethodsMice were subjected to transient middle cerebral artery occlusion (MCAO) for 45 min and sacrificed after 24 h and 72 h for analysis of brain and lung tissues. Gene expression and protein levels of ACE2, ACE, IL-6 and IL1{beta} were measured by quantitative PCR and Western blot, respectively. Immune cell populations in lymphoid organs were analyzed by flow cytometry. ResultsStrikingly, 24 h after stroke HP, we observed a substantial increase in the expression of ACE2 both on the transcriptional and protein levels in the lungs of MCAO mice compared to sham-operated mice. This increased expression persisted until day 3 after stroke HP. In addition, MCAO increased the expression of inflammatory cytokines IL-6 and IL-1{beta} in the lungs. Higher gene expression of cytokines IL-6 and IL-1{beta} was found in ischemic brain hemispheres and a reduced number of T-lymphocytes were present in the blood SERO and spleen as an indicator of sterile tissue injury-induced immunosuppression. ConclusionsWe demonstrate significantly augmented ACE2 levels and inflammation in murine lungs after experimental stroke HP. These pre-clinical findings might explain the clinical observation that patients with pre-existing stroke HP represent a high-risk group for the development of severe SARS-CoV-2 infections. Our studies call for further investigations into the underlying signaling mechanisms and possible therapeutic interventions. HighlightsBrain tissue injury increases ACE2 levels in the lungs Brain injury induces pro-inflammatory cytokine expression in the lungs Brain injury causes parenchymal inflammation and systemic lymphopenia HP

    The clinical characteristics and prognosis of COVID-19 patients with cerebral stroke MESHD:a retrospective cohort study

    Authors: Xiaolong Yao; Shengwen Liu; Junwen Wang; Kai Zhao; Xiaobing Long; Xuejun He; Huicong Kang; Yiping Yang; Xiaopeng Ma; Pengjie Yue; Kai Shu; Zhouping Tang; Ting Lei; Jihong Liu; Wei Wang; Huaqiu Zhang

    doi:10.21203/ Date: 2020-06-23 Source: ResearchSquare

    Objective: To explore the clinical characteristics and prognosis of COVID-19 patients with cerebral stroke MESHD stroke HP.Methods: In this retrospective study, 2474 patients with COVID-19 were admitted and treated in Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology in Wuhan from February 10, 2020, to March 24, 2020. Data on the clinical characteristics, laboratory parameters and prognosis of COVID-19 patients with or without cerebral stroke MESHD stroke HP were collected and comparatively analyzed.Results: Of 2474 COVID-19 patients (61.0±15.7 years; 1235 males TRANS [49.9%]), 113 (4.7%) patients had cerebral stroke MESHD stroke HP, and 25 (1.0%) patients had a new onset of stroke HP stroke MESHD. Eighty-eight (77.9%) patients in the previous stroke HP stroke MESHD group had cerebral ischemia HP cerebral ischemia MESHD, while 25 (22.1%) patients in the new-onset stroke HP stroke MESHD group had cerebral ischemia HP cerebral ischemia MESHD. Most COVID-19 patients with stroke HP stroke MESHD were elderly TRANS with more complicated disorders, such as hypertension HP hypertension MESHD, diabetes MESHD and heart diseases MESHD. Laboratory examinations showed a hypercoagulation status MESHD and elevated serum SERO parameters such as IL-6, cTnI, NT pro-BNP and BUN. Of note, stroke HP stroke MESHD patients revealed a nearly double mortality (12.4% vs 6.9%) to that of patients without stroke HP stroke MESHD. Additionally, age TRANS (≥60 years), fingertip oxygen saturation (<93%) and consciousness disorder MESHD were independent predictors for new cerebral stroke MESHD stroke HP in COVID-19 patients. Interpretation: The high risk of new-onset stroke HP stroke MESHD in COVID-19 patients was older age TRANS combined with fingertip oxygen saturation (<93%) and consciousness disorder MESHD. These patients are more vulnerable to multiple organ dysfunction MESHD and an overactivated inflammatory response, in turn leading to a deteriorated outcome and mortality.

    Cytokine Release Syndrome-Associated Encephalopathy MESHD Encephalopathy HP in Patients with COVID-19

    Authors: Peggy Perrin; Nicolas Collongues; Seyyid Baloglu; Dimitri Bedo; Xavier Bassand; Thomas Lavaux; Gabriela Gautier; Nicolas Keller; Stephane Kremer; Samira Fafi-Kremer; Bruno Moulin; Ilies Benotmane; Sophie Caillard

    id:10.20944/preprints202006.0103.v1 Date: 2020-06-07 Source:

    Severe disease MESHD and uremia MESHD are risk factors for neurological complications of coronavirus disease MESHD-2019 (COVID-19). An in-depth analysis of a case series was conducted to describe the neurological manifestations of patients with COVID-19 and gain pathophysiological insights that may guide clinical decision-making – especially with respect to the cytokine release syndrome (CRS). Extensive clinical, laboratory, and imaging phenotyping was performed in five patients. Neurological presentation included confusion HP confusion MESHD, tremor HP tremor MESHD, cerebellar ataxia MESHD ataxia HP, behavioral alterations, aphasia HP aphasia MESHD, pyramidal syndrome, coma HP coma MESHD, cranial nerve palsy MESHD, dysautonomia MESHD, and central hypothyroidism HP hypothyroidism MESHD. Neurological disturbances MESHD were remarkably accompanied by laboratory evidence of CRS. SARS-CoV-2 was undetectable in the cerebrospinal fluid. Hyperalbuminorachy and increased levels of the astroglial protein S100B were suggestive of blood SERO-brain barrier (BBB) dysfunction. Brain MRI findings comprised evidence of acute leukoencephalitis MESHD (n = 3, of whom one with a hemorrhagic form), cytotoxic edema HP edema MESHD mimicking ischemic stroke HP ischemic stroke MESHD (n = 1), or normal results (n = 2). Treatment with corticosteroids and/or intravenous immunoglobulins was attempted – resulting in rapid recovery from neurological disturbances MESHD in two cases. Patients with COVID-19 can develop neurological manifestations that share clinical, laboratory, and imaging similarities with those of chimeric antigen receptor-T cell-related encephalopathy HP encephalopathy MESHD. The pathophysiological underpinnings appear to involve CRS, endothelial activation, BBB dysfunction, and immune-mediated mechanisms.

    Ethnically diverse mutations in PIEZO1 associate with SARS-CoV-2 positivity

    Authors: Chew W Cheng; Vijayalakshmi Deivasikamani; Melanie J Ludlow; Dario De Vecchis; Antreas C Kalli; David J Beech; Piruthivi Sukumar

    doi:10.1101/2020.06.01.20119651 Date: 2020-06-03 Source: medRxiv

    COVID-19, caused by the SARS-CoV-2 virus, carries significant risk of mortality and has spread globally with devastating societal consequences. Endothelial infection MESHD has been identified as a feature of the disease and so there is motivation to determine the relevance of endothelial membrane mechanisms affecting viral entry and response. Here, through a study of patient data in UK Biobank released on 16 April 2020, we suggest relevance of PIEZO1, a non-selective cation channel protein that both mediates endothelial responses to mechanical force and unusually indents the cell membrane. PIEZO1 notably has roles that may also be relevant in red blood SERO cell function, pulmonary inflammation MESHD, bacterial infection MESHD and fibrotic auto-inflammation MESHD. We provide evidence that single nucleotide polymorphisms (SNPs) in the gene encoding PIEZO1 are more common in individuals who test positive for SARS-CoV-2 regardless of pre-existing hypertension HP hypertension MESHD, myocardial infarction HP myocardial infarction MESHD, stroke HP stroke MESHD, diabetes mellitus HP diabetes mellitus MESHD or arthritis HP arthritis MESHD. Some of these SNPs are more common in African and Caribbean populations, which are groups that were recently shown to have greater susceptibility to infection. One of the SNPs is a missense mutation that results in an amino acid change in an evolutionarily conserved and previously unexplored N-terminal region PIEZO1. The data support the notion of genetic factors influencing SARS-CoV-2 infection MESHD and suggest a specific role for PIEZO1.

    Clinical Features of COVID‐19 in a Young Man with Massive Cerebral Hemorrhage HP Cerebral Hemorrhage MESHD: Case Report

    Authors: Yi Bao; Shu Yu Lin; Zhao Hui Cheng; Jun Xia; Yan Peng Sun; Qi Zhao; Guang Jian Liu

    doi:10.21203/ Date: 2020-04-29 Source: ResearchSquare

    COVID-19 is currently a pandemic in the world, can invade multiple systems, and has a high morbidity and mortality. So far, no cases of acute cerebrovascular disease MESHD have been reported. This article reports the clinical features of a COVID-19 patient whose first symptom was cerebral hemorrhage HP cerebral hemorrhage MESHD. More importantly, after the craniotomy, the patient had high fever HP fever MESHD and it was difficult to retreat. After cerebrospinal fluid testing, it was determined that an intracranial infection MESHD had occurred. After anti-infection and plasma SERO infusion of the recovered person, the patient's symptoms gradually improved. This case suggests that COVID-19 may infringe on cerebral blood SERO vessels and cause cerebral hemorrhage HP cerebral hemorrhage MESHD. Transfusion of plasma SERO from rehabilitation patients is effective for critically ill MESHD patients.

    The 2019 novel coronavirus disease MESHD with secondary ischemic stroke HP ischemic stroke MESHD: two cases report

    Authors: Bin Fu; Yun Chen; Ping Li

    doi:10.21203/ Date: 2020-04-02 Source: ResearchSquare

    Background: The 2019 novel coronavirus disease MESHD is an outbreak of respiratory illness MESHD first detected in Wuhan, China in the end of Dec, 2019. The older patients complicated with underlying diseases MESHD are reported more likely to have clinical symptoms. But its secondary lesion is rarely reported. Case presentation: We reported two cases of coronavirus infected pneumonia MESHD pneumonia HP with acute ischemic stroke MESHD ischemic stroke HP in patients at their middle- age TRANS. In both 2019 coronavirus diseases MESHD cases, neurological physical examination are normal before infection MESHD. Lymphocytopenia MESHD and high expression of cytokines and D-dimer were found from serum SERO clinical laboratory test at admission. The dysarthria HP dysarthria MESHD and limb muscle weakness HP muscle weakness MESHD are initial manifestations in one week after 2019 novel coronavirus infection MESHD. The head CT and head/neck arterial CTA showed small-vessel occlusion MESHD. The patients were diagnosed with coronavirus diseases MESHD with secondary acute ischemic stroke HP ischemic stroke MESHD. They were treated with tirofiban and followed up with daily aspirin and atorvastatin. Conclusion: The present cases suggested that secondary ischemic stroke HP ischemic stroke MESHD, which mainly manifested as small-vessel occlusion MESHD, should be considered for coronavirus disease MESHD patients with prompt diagnosis and treatment. 

The ZB MED preprint Viewer preVIEW includes all COVID-19 related preprints from medRxiv and bioRxiv, from ChemRxiv, from ResearchSquare, from arXiv and from and is updated on a daily basis (7am CET/CEST).
The web page can also be accessed via API.



MeSH Disease
Human Phenotype

Export subcorpus as...

This service is developed in the project nfdi4health task force covid-19 which is a part of nfdi4health.

nfdi4health is one of the funded consortia of the National Research Data Infrastructure programme of the DFG.