Fig. 6

Mitochondrial impairment and its potential involvement in long-haul COVID. SARS-CoV2 directly infects mitochondria via injecting its RNA, manipulates mitochondrial gene synthesis machinery, and alters mitochondrial metabolomes. The impairment can be the release of pro-apoptotic molecules such as Bax, Bad, and cytochrome C; reversal of membrane potential; downregulation of β-oxidation and electron transport mechanism causing impaired ATP synthesis; induction of mitochondria-independent cytosolic glycolysis resulting in increased lactate synthesis. All these events trigger mitochondrial loss and eventually fatigue