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

Area of Science:

• Pathology
• Virology
• Biochemistry

Background:

• Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection causes multi-organ failure, cytokine storm, and septic shock.
• The virus's N protein inhibits mitochondrial interferon production, leading to organelle hijacking.

Purpose of the Study:

• To investigate how SARS-CoV-2 commandeers mitochondrial machinery for viral survival.
• To determine the link between mitochondrial dysfunction, altered serum parameters, and nitrosative stress (NSS) in COVID-19.

Main Methods:

• Prospective cohort study of 15 postmortem COVID-19 patients.
• Analysis of six mitochondrial function markers (COX II, COX IV, MnSOD, nitrotyrosine, Bcl-2, caspase-9) using immune colloidal gold technique in lung, heart, and liver tissues.
• Evaluation of biometric laboratory results.

Main Results:

• Significant alterations observed in serum parameters including hemoglobin, platelets, creatinine, glucose, C-reactive protein, D-dimer, ferritin, fibrinogen, Ca²⁺, K⁺, lactate, and troponin.
• Detected changes in mitochondrial structure and function, including markers of nitrosative stress (NSS).
• Correlation between laboratory findings and mitochondrial damage.

Conclusions:

• COVID-19-induced multi-organ dysfunction is partly attributed to mitochondrial damage.
• Mitochondrial dysfunction contributes to an inflammatory state, NSS, sepsis cascade activation, and increased mortality in COVID-19 patients.