Abstract
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection leads to multiorganic failure associated with a cytokine storm and septic shock. The virus evades the mitochondrial production of interferons through its N protein. From that moment on, SARS-CoV-2 hijacks 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, 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, kidney 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 of the mitochondrial structure and function. The multiorganic 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 the elevation of NSS. NSS activates the sepsis cascade and contributes to the increased mortality in COVID-19 patients.
Platelets Affect the Structure and Function of C-Reactive Protein