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HGNC Genes

SARS-CoV-2 proteins

ProteinN (1)


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    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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