Publication: The kidnapping of mitochondrial function associated with the SARS-CoV-2 infection
Authors
Soria-Castro, Elizabeth ; Soto, María Elena ; Guarner-Lans, Verónica ; Rojas, Gustavo ; Perezpeña-Diazconti, Mario ; Críales-Vera, Sergio A ; Manzano Pech, Linaloe ; Pérez-Torres, Israel
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-354
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info:eu-repo/semantics/article
Description
Abstract
Infection by the Severe Acute Respiratory
Syndrome Coronavirus 2 (SARS-CoV-2) leads to multiorgan failure associated with a cytokine storm and septic
shock. The virus evades the mitochondrial production of
interferons through its N protein and, from that moment
on, it hijacks the functions of these organelles. The aim
of this study was to show how the virus kidnaps the
mitochondrial machinery for its benefit and survival,
leading to alterations of serum parameters and to
nitrosative stress (NSS). In a prospective cohort of 15
postmortem patients who died from COVID-19, six
markers of mitochondrial function (COX II, COX IV,
MnSOD, nitrotyrosine, Bcl-2 and caspase-9) were
analyzed by the immune colloidal gold technique in
samples from the lung, heart, and liver. Biometric
laboratory results from these patients showed alterations
in hemoglobin, platelets, creatinine, urea nitrogen,
glucose, C-reactive protein, albumin, D-dimer, ferritin,
fibrinogen, Ca2+, K+, lactate and troponin. These
changes were associated with alterations in the
mitochondrial structure and function. The multi-organ
dysfunction present in COVID-19 patients may be
caused, in part, by damage to the mitochondria that
results in an inflammatory state that contributes to NSS,
which activates the sepsis cascade and results in
increased mortality in COVID-19 patients.
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Citation
Histology and Histopathology Vol. 36, nº9 (2021)
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