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e.XuM.RenQ.FanY.LiuB.ChenJ.et al (2022)

These results may be further supported by the observations of Bahmani et al

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This oxidative environment causes mtDNA lesions, mutations, and deletions ( Tat (transactivator of transcription) protein, even in the absence of productive infection, can enter mitochondria and inhibit the expression and function of TFAM (Mitochondrial transcription factor A), thereby impairing mtDNA replication and transcription and reducing the expression of mtDNA-encoded ETC subunits ( 4.3 Consequences of mtDNA damage: from bioenergetic crisis to immune exhaustion mtDNA mutations and depletion impair the synthesis of essential ETC components, resulting in defective OXPHOS, reduced ATP synthesis, collapse of the mitochondrial membrane potential (m), and accumulation of metabolic intermediates due to TCA cycle disruption and compensatory glycolysis