Putative role of mitochondria in SARS-CoV-2 mediated brain dysfunctions: a prospect

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the COVID-19 pandemic. Though the virus primarily damages the respiratory and cardiovascular systems after binding to the host angiotensin-converting enzyme 2 (ACE2) receptors, it has the potential to affect all major organ systems, including the human nervous system. There are multiple clinical reports of anosmia, dizziness, headache, nausea, ageusia, encephalitis, demyelination, neuropathy, memory loss, and neurological complications in SARS-CoV-2 infected individuals. Though the molecular mechanism of these brain dysfunctions during SARS-CoV-2 infection is elusive, the mitochondria seem to be an integral part of this pathogenesis. Emerging research findings suggest that the dysfunctional mitochondria and associated altered bioenergetics in the infected host cells lead to altered energy metabolism in the brain of Covid-19 patients. The interactome between viral proteins and mitochondrial proteins during Covid-19 pathogenesis also provides evidence for the involvement of mitochondria in SARS-CoV-2-induced brain dysfunctions. The present review discusses the possible role of mitochondria in disturbing the SARS-CoV-2 mediated brain functions, with the potential to use this information to prevent and treat these impairments.