Corpus overview


Overview

MeSH Disease

Human Phenotype

Edema (3)

Pneumonia (2)


Transmission

There are no transmission terms in the subcorpus


Seroprevalence

There are no seroprevalence terms in the subcorpus

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    Endothelial Cells and SARS-CoV-2: An Intimate Relationship

    Authors: Lucas Barbosa; Thaynan Lopes; Luanna Araujo; Luciane Rosario; Valeria Ferrer

    id:10.20944/preprints202010.0214.v1 Date: 2020-10-12 Source: Preprints.org

    Angiotensin-converting enzyme 2 (ACE2) is an important player of the renin-angiotensin-aldosterone system (RAAS) in regulating the conversion of angiotensin II into angiotensin (1-7). While expressed on the surface of human cells, such as lung, heart, kidney, neurons, and endothelial cells (EC), ACE2 is the entry receptor for SARS-CoV-2. Here, we would like to highlight that ACE2 is predominant on the EC membrane. Many of coronavirus disease MESHD 2019 (COVID-19) symptoms have been associated with the large recruitment of immune cells, directly affecting EC. Additionally, cytokines, hypoxia MESHD, and complement activation can trigger the activation of EC leading to the coagulation cascade. The EC dysfunction plus the inflammation MESHD due to SARS-CoV-2 infection MESHD may lead to abnormal coagulation MESHD, actively participating in thrombo-inflammatory processes resulting in vasculopathy MESHD and indicating poor prognosis in patients with COVID-19. Considering the intrinsic relationship between EC and the pathophysiology of SARS-CoV-2, EC-associated therapies such as anticoagulants, fibrinolytic drugs, immunomodulators, and molecular therapies have been proposed. In this review, we will discuss the role of EC in the lung inflammation MESHD and edema HP edema MESHD, in the disseminate coagulation process, ACE2 positive cancer MESHD patients, and current and future EC-associated therapies to treat COVID-19.

    STAT2 signaling as double-edged sword restricting viral dissemination but driving severe pneumonia HP pneumonia MESHD in SARS-CoV-2 infected MESHD hamsters

    Authors: Robbert Boudewijns; Hendrik Jan Thibaut; Suzanne J.F. Kaptein; Rong Li; Valentijn Vergote; Laura Seldeslachts; Carolien De Keyzer; Lindsey Bervoets; Sapna Sharma; Johan Van Weyenbergh; Laurens Liesenborghs; Ji Ma; Sander Jansen; Dominique Van Looveren; Thomas Vercruysse; Dirk Jochmans; Xinyu Wang; Erik Martens; Kenny Roose; Dorien De Vlieger; Bert Schepens; Tina Van Buyten; Sofie Jacobs; Yanan Liu; Joan Martí-Carreras; Bert Vanmechelen; Tony Wawina-Bokalanga; Leen Delang; Joana Rocha-Pereira; Lotte Coelmont; Winston Chiu; Pieter Leyssen; Elisabeth Heylen; Dominique Schols; Lanjiao Wang; Lila Close; Jelle Matthijnssens; Marc Van Ranst; Veerle Compernolle; Georg Schramm; Koen Van Laere; Xavier Saelens; Nico Callewaert; Ghislain Opdenakker; Piet Maes; Birgit Weynand; Christopher Cawthorne; Greetje Vande Velde; Zhongde Wang; Johan Neyts; Kai Dallmeier

    doi:10.1101/2020.04.23.056838 Date: 2020-04-24 Source: bioRxiv

    Introductory paragraphSince the emergence of SARS-CoV-2 causing COVID-19, the world is being shaken to its core with numerous hospitalizations and hundreds of thousands of deaths. In search for key targets of effective therapeutics, robust animal models mimicking COVID-19 in humans are urgently needed. Here, we show that productive SARS-CoV-2 infection MESHD in the lungs of mice is limited and restricted by early type I interferon responses. In contrast, we show that Syrian hamsters are highly permissive to SARS- CoV-2 and develop bronchopneumonia MESHD and a strong inflammatory response in the lungs with neutrophil infiltration and edema HP edema MESHD. Moreover, we identify an exuberant innate immune response as a key player in pathogenesis, in which STAT2 signaling plays a dual role, driving severe lung injury MESHD on the one hand, yet restricting systemic virus dissemination on the other. Finally, we assess SARS-CoV- 2-induced lung pathology in hamsters by micro-CT alike used in clinical practice. Our results reveal the importance of STAT2-dependent interferon responses in the pathogenesis and virus control during SARS-CoV-2 infection MESHD and may help rationalizing new strategies for the treatment of COVID-19 patients.

    Pulmonary Pathology of Early Phase 2019 Novel Coronavirus (COVID-19) Pneumonia HP in Two Patients with Lung Cancer MESHD

    Authors: Sufang Tian; Weidong Hu; Li Niu; Huan Liu; Haibo Xu; Shu-Yuan Xiao

    id:10.20944/preprints202002.0220.v2 Date: 2020-03-02 Source: Preprints.org

    There is currently a lack of pathologic data on the novel coronavirus ( SARS-CoV-2) pneumonia MESHD pneumonia HP, or COVID-19, from autopsy or biopsy. Two patients who recently underwent lung lobectomies for adenocarcinoma MESHD were retrospectively found to have had COVID-19 at the time of surgery. These two cases thus provide important first opportunities to study the pathology of COVID-19. Pathologic examinations revealed that, apart from the tumors MESHD, the lungs of both patients exhibited edema HP edema MESHD, proteinaceous exudate, focal reactive hyperplasia MESHD of pneumocytes with patchy inflammatory cellular infiltration, and multinucleated giant cells. Hyaline membranes were not prominent. Since both patients did not exhibit symptoms of pneumonia HP pneumonia MESHD at the time of surgery, these changes likely represent an early phase of the lung pathology of COVID-19 pneumonia HP pneumonia MESHD.

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MeSH Disease
Human Phenotype
Transmission
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