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Related Concept Videos

The Electron Transport Chain01:30

The Electron Transport Chain

The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...

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Related Experiment Video

Updated: Jun 5, 2026

Oxygen-Independent Assays to Measure Mitochondrial Function in Mammals
05:59

Oxygen-Independent Assays to Measure Mitochondrial Function in Mammals

Published on: May 19, 2023

Mitochondrial OXPHOS restricts SARS-CoV-2 replication.

Yentli E Soto Albrecht1,2,3,4, Ryan M Morrow1, Devin Kenney3,4

  • 1Center for Mitochondrial and Epigenomic Medicine, Children's Hospital of Philadelphia, Philadelphia, PA, USA.

Science Advances
|June 3, 2026
PubMed
Summary
This summary is machine-generated.

Mitochondrial oxidative phosphorylation (OXPHOS) inhibits SARS-CoV-2 replication. Inhibiting OXPHOS boosts viral production, while restoring it reduces virus levels, highlighting metabolic balance in controlling infection.

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Using Isolated Mitochondria from Minimal Quantities of Mouse Skeletal Muscle for High throughput Microplate Respiratory Measurements

Published on: October 30, 2015

Area of Science:

  • Virology
  • Cell Biology
  • Metabolic Research

Background:

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) manipulates host cell metabolism for replication.
  • The role of mitochondrial oxidative phosphorylation (OXPHOS) in SARS-CoV-2 production remains unclear.
  • Mitochondrial DNA (mtDNA) encodes essential components for OXPHOS and mitochondrial protein synthesis.

Purpose of the Study:

  • To investigate the impact of OXPHOS on SARS-CoV-2 replication.
  • To determine if OXPHOS inhibition affects viral production and replication dynamics.
  • To elucidate the role of metabolic balance in regulating SARS-CoV-2 infection.

Main Methods:

  • Utilized human ACE2-expressing A549 lung cells, including mtDNA-depleted (ρ0) cells.
  • Inhibited OXPHOS using mtDNA depletion, chloramphenicol (CAP), and chemical inhibitors.
  • Assessed viral production, replication center formation, and infectious particle release.
  • Analyzed glycolytic capacity and innate immune pathway activation.
  • Restored OXPHOS by reintroducing mtDNA into ρ0 cells.

Main Results:

  • SARS-CoV-2 production increased 5- to 100-fold upon OXPHOS inhibition.
  • OXPHOS inhibition accelerated viral replication and particle release by approximately 2 hours.
  • Enhanced viral replication correlated with increased glycolytic capacity, not innate immunity.
  • Restoring OXPHOS impaired viral replication and reversed metabolic changes.

Conclusions:

  • Mitochondrial oxidative phosphorylation (OXPHOS) exerts an antiviral effect against SARS-CoV-2.
  • Metabolic balance, specifically the interplay between OXPHOS and glycolysis, is critical for regulating viral replication.
  • Targeting OXPHOS could be a potential strategy for managing SARS-CoV-2 infection.