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MeSH Disease

Human Phenotype

Transmission

Seroprevalence

antibody (3)

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    Kawasaki Disease MESHD Outbreak in Children TRANS During COVID-19 Pandemic.

    Authors: Ewelina Gowin; Jacek Wysocki; Magdalena Frydrychowicz; Danuta Januszkiewicz-Lewandowska

    doi:10.21203/rs.3.rs-70123/v1 Date: 2020-09-01 Source: ResearchSquare

    BackgroundIn response to the recent information about the outbreak of Kawasaki disease MESHD ( KD MESHD) in children TRANS connected to SARS-Cov-2 pandemic, we would like to present a group of six patients hospitalized from March to May 2020 with an inflammatory disease similar to KD MESHD. Findings There were four girls and two boys, aged TRANS from 15 months to 16 years. They all presented with fever HP fever MESHD lasting at least five days, irritability HP irritability MESHD, bilateral nonexudative conjunctivitis HP conjunctivitis MESHD, lymphadenopathy, mucus membrane changes, rash MESHD, edema HP edema MESHD.Neither the patients nor the other members of the patients' households had a positive history of COVID-19 infection MESHD. None of the six children TRANS had a positive PCR result for SARS-CoV-2 or a positive results for antibodies to SARS-CoV-2 SERO. All patients received empiric antibiotic therapy. Four patients were diagnosed with KD MESHD. Three children TRANS received standard treatment. One boy did not respond and received an additional 14-days course of methylprednisolone.In two girls, the diagnosis of KD MESHD was not made. All patients survived ConclusionFinding a correlation with the Covid-19 pandemic is difficult regarding the situation in our country. According to ECDC, in May 2020 Poland wass still before the peak of the epidemy. The intention of this article is to report that increased hospitalization of children TRANS with the inflammatory syndrome MESHD is also observed in countries with low levels of transmission TRANS of the SARS-Cov-2 virus. Our observation may broaden the knowledge of new inflammatory syndrome MESHD, which is not necessarily caused by SARS-Cov-2 but may be worsened by co-infection MESHD.

    Myocardial Injury MESHD in Post Mortem Biopsies of Patients with COVID-19

    Authors: Camila Hartmann; Anna Flavia dos Santos Miggiolaro; Jarbas da Silva Motta Junior; Lucas Baena Carstens; Caroline Busatta Vaz De Paula; Larissa Hermann de Souza Nunes; Gustavo Lenci Marques; Lidia Zytinsky Moura; Jose Rocha Faria Neto; Lucia de Noronha; Cristina Pellegrino Baena

    doi:10.21203/rs.3.rs-45192/v1 Date: 2020-07-17 Source: ResearchSquare

    Background: Myocardial injury MESHD is significantly and independently associated with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury MESHD in COVID-19 is still not clear, and cardiac involvement by SARS-CoV-2 remains a major challenge worldwide.Aim: This histopathological and immunohistochemical study seeks to clarify the pathogenesis of myocardial injury MESHD in COVID-19.Methods: Postmortem minimally invasive autopsies were performed in two patients who died from COVID-19, and the myocardium samples were compared to a control patient. Immunohistochemistry (IHC) staining was performed using monoclonal antibodies SERO against the following targets: caspase-1, ICAM-1, TNF-α, IL-4, IL-6, CD163, TGF-β, MMP-9, type 1 and type 3 collagen.Results: The histopathological analysis showed severe pericellular interstitial edema HP edema MESHD surrounding each of the cardiomyocytes. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-4, IL-6, CD163, MMP-9 and type 3 collagen in the COVID-19 patients compared to the control. On the other hand, no difference from the control was observed in expression of TNF-α, TGF-β and type 1 collagen. Conclusion: Our findings point to a pathogenesis related with pyroptosis leading to endothelial disfunction. The subsequent inflammation MESHD with associated interstitial edema HP edema MESHD could explain the myocardial disfunction and arrythmias MESHD in COVID-19 patients. The presence of Th2 response, MMP-9 and type-3 collagen suggests progression to myocardial fibrosis HP myocardial fibrosis MESHD in the long term.

    Functional pangenome analysis provides insights into the origin, function and pathways to therapy of SARS-CoV-2 coronavirus MESHD

    Authors: Intikhab Alam; Allan K Kamau; Maxat Kulmanov; Stefan T Arold; Arnab T Pain; Takashi Gojobori; Carlos M. Duarte

    doi:10.1101/2020.02.17.952895 Date: 2020-02-21 Source: bioRxiv

    The spread of the novel coronavirus (SARS-CoV-2) has triggered a global emergency, that demands urgent solutions for detection and therapy to prevent escalating health, social and economic impacts. The spike protein (S) of this virus enables binding to the human receptor ACE2, and hence presents a prime target for vaccines preventing viral entry into host cells1. The S proteins from SARS-CoV-1 and SARS-CoV-2 MESHD are similar2, but structural differences in the receptor binding domain (RBD) preclude the use of SARS-CoV-1-specific neutralizing antibodies SERO to inhibit SARS-CoV-23. Here we used comparative pangenomic analysis of all sequenced Betacoronaviruses to reveal that, among all core gene clusters present in these viruses, the envelope protein E shows a variant shared by SARS and SARS-Cov2 with two completely-conserved key functional features, an ion-channel and a PDZ-binding Motif (PBM). These features trigger a cytokine storm that activates the inflammasome, leading to increased edema HP edema MESHD in lungs causing the acute respiratory distress syndrome MESHD respiratory distress HP syndrome ( ARDS MESHD)4-6, the leading cause of death MESHD in SARS-CoV-1 and SARS-CoV-2 infection7 MESHD,8. However, three drugs approved for human use may inhibit SARS-CoV-1 and SARS-CoV-2 Protein E, either acting upon the ion channel (Amantadine and Hexamethylene amiloride9,10) or the PBM (SB2035805), thereby potentially increasing the survival of the host, as already demonstrated for SARS-CoV-1in animal models. Hence, blocking the SARS protein E inhibits development of ARDS in vivo. Given that our results demonstrate that the protein E subcluster for the SARS clade is quasi-identical for the key functional regions of SARS-CoV-1 and SARS-CoV-2, we conclude that use of approved drugs shown to act as SARS E protein inhibitors can help prevent further casualties from COVID-2019 while vaccines and other preventive measures are being developed.

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