Decoding SARS-CoV-2 hijacking of host mitochondria in COVID-19 pathogenesis

There is growing evidence that the SARS CoV 2 virus can directly manipulate mitochondrial function to evade host cell immunity and facilitate virus replication and COVID-19 disease. Manipulations of host mitochondria can release mitochondrial DNA (mtDNA) in the cytoplasm and activate mtDNA-induced inflammasome and suppress innate and adaptive immunity. A decline in ACE2 function in aged individuals, coupled with the age-associated decline in mitochondrial functions resulting in chronic metabolic disorders like diabetes or cancer, may make the host more vulnerable to infection and health complications to mortality. These are important findings for those infected with SARS CoV 2, either through natural infection, or as the result of receiving the COVID injections which tell the body to repeatedly reproduce the spike protein responsible for these impacts on the cell’s mitochondria.

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