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

xlomafota13 shared this article with you from Inoreader The kidnapping of mitochondrial function associated with the SARS-CoV-2 infection Via Cellular and Molecular Biology Histol Histopathol. 2021 Jun 16:18354. doi: 10.14670/HH-18-354. Online ahead of print. ABSTRACT Infection by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) leads to multi-organ 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. PMID:34132382 | DOI:10.14670/HH-18-354 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.