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MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

ProteinS (1)

ProteinN (1)


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    Pyroptosis of syncytia formed by fusion of SARS-CoV-2 Spike PROTEIN SARS-CoV-2 Spike MESHD and ACE2 HGNC expressing cells

    Authors: Huabin Ma; Zhoujie Zhu; Huaipeng Lin; Shanshan Wang; Peipei Zhang; Yanguo Li; Long Li; Jinling Wang; Yufen Zhao; Jiahuai Han

    doi:10.1101/2021.02.25.432853 Date: 2021-02-25 Source: bioRxiv

    SARS-Cov-2 infected cells fused with the ACE2 HGNC-positive neighboring cells forming syncytia. However, the effect of syncytia in disease development is largely unknown. We established an in vitro cell-cell fusion system and used it to mimic the fusion of SARS-CoV-2 infected MESHD cells with ACE2 HGNC-expressing cells to form syncytia. We found that Caspase-9 HGNC was activated after syncytia formation, and Caspase-3/7 was activated downstream of Caspase-9 HGNC, but it triggered GSDME-dependent pyroptosis rather than apoptosis. What is more, single cell RNA-sequencing data showed that both ACE2 HGNC and GSDME were expression in alveolar type MESHD 2 cells in human lung. We propose that pyroptosis is the fate of syncytia formed by SARS-CoV-2 infected host MESHD cells and ACE2 HGNC-positive cells, which indicated that lytic death of syncytia MESHD may contribute to the excessive inflammatory responses in severe COVID-19 MESHD patients.

    The kidnapping of mitochondrial function associated to the SARS-CoV-2 infection MESHD

    Authors: Elizabeth Soria-Castro; María Elena Soto; Verónica; Gustavo Rojas; Mario Perezpeña-Diazconti; Sergio A Críales-Vera; Linaloe Manzano Pech; Israel Pérez-Torres

    doi:10.21203/rs.3.rs-137853/v1 Date: 2020-12-29 Source: ResearchSquare

    Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection leads to multiorganic failure MESHD associated with a cytokine storm and septic shock MESHD. The virus evades the mitochondrial production of interferons through its N protein PROTEIN. From that moment on, SARS-CoV-2 hijacks MESHD the functions of this organelle. The aim of this study was to show how the virus kidnaps the mitochondrial machinery for its benefit and survival, altering serum parameters and leading to nitrosative stress (NSS). In a prospective cohort of 15 postmortem patients who died from COVID-19 MESHD, six markers of mitochondrial function; COX II, COX IV HGNC, MnSOD HGNC, nitrotyrosine, Bcl-2 HGNC and caspase-9 HGNC were analyzed by the immune colloidal gold technique in samples from the lung, heart, kidney and liver. Biometric laboratory results from these patients showed alterations in hemoglobin, platelets, creatinine, urea nitrogen, glucose, C-reactive protein HGNC, albumin, D-dimer, ferritin, fibrinogen HGNC, Ca2+, K+, lactate and troponin. These changes were associated with alterations of the mitochondrial structure and function. The multiorganic dysfunction MESHD present in COVID-19 MESHD patients may be caused in part by damage to the mitochondria that results in an inflammatory state that contributes to the elevation of NSS. NSS activates the sepsis MESHD cascade and contributes to the increased mortality in COVID-19 MESHD patients.

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MeSH Disease
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SARS-CoV-2 Proteins


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