Pathophysiological involvement of host mitochondria in SARS-CoV-2 infection that causes COVID-19: a comprehensive

Chandan Bhowal1, Sayak Ghosh1, Debapriya Ghatak2

  • 1Amity Institute of Biotechnology, Amity University, Plot No: 36, 37 & 38, Major Arterial Road, Action Area II, Kadampukur Village, Newtown, Kolkata, 700135, West Bengal, India.

Insights

SARS-CoV-2 infection alters mitochondria, impacting redox balance, inflammation, and antiviral responses. Targeting these mitochondrial changes may offer new COVID-19 therapies.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • SARS-CoV-2 causes COVID-19, prompting research into therapeutic targets.
  • Mitochondria are crucial cellular organelles susceptible to viral infections.
  • Mitochondrial dysfunction is increasingly implicated in viral pathogenesis.

Purpose of the Study:

  • To review and synthesize recent findings on SARS-CoV-2's impact on mitochondrial function.
  • To explore the role of mitochondria in COVID-19 pathogenesis and prognosis.
  • To identify potential therapeutic strategies targeting mitochondrial alterations.

Main Methods:

  • Literature review of in vitro, pre-clinical, and clinical studies.
  • Analysis of SARS-CoV-2 interactions with mitochondrial antiviral signaling (MAVS).
  • Examination of viral open reading frames (ORFs) effects on mitochondrial regulation.

Main Results:

  • SARS-CoV-2 infection alters mitochondrial redox homeostasis, morphology, and bioenergetics.
  • Viral proteins (M, ORF-9b, ORF-6) inhibit MAVS, impairing innate antiviral responses.
  • Mitochondrial dysfunction, increased mtROS, and NLRP3 inflammasome activation are observed, particularly in aged individuals.

Conclusions:

  • Mitochondria play a significant role in COVID-19 pathogenesis and disease progression.
  • Mitochondrial alterations represent a promising avenue for novel therapeutic interventions.
  • Understanding mitochondrial dynamics in SARS-CoV-2 infection is key for developing effective treatments.

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