Could cellular energy factories hold the key to understanding Long COVID?

SARS-CoV-2 virus appears to disrupt genes in cellular energy factories called mitochondria, interfering with metabolism.

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Human cells under the microscope.
 

 

Since the beginning of the COVID-19 pandemic, scientists have puzzled over how the virus manages to wreak such long-term havoc on people’s internal organs. Now scientists have discovered that the virus hinders the normal function of mitochondria, tiny energy-producing factories within our cells. The discovery, published in Science Translational Medicine, could ultimately lead to new ways of treating immediate and ongoing COVID-19 symptoms by targeting mitochondrial function.

While further studies are needed to confirm this in people with Long COVID, the team speculated that therapies targeting mitochondrial function might reduce COVID-19 symptoms, both during the early stages of infection and in patients living with chronic disease.

Mitochondria are tiny structures found in every cell that generate the energy necessary to power our bodies. Previous studies have suggested that SARS-CoV-2 proteins can bind to mitochondria in our cells, potentially disrupting their function.

To delve deeper, a consortium of researchers led by Dr Douglas C. Wallace at Childrens Hospital of Philadelphia, US, and Dr Afshin Beheshti of the COVID-19 International Research Team in Medford US, examined tissue samples from living and deceased COVID-19 patients looking at how mitochondrial gene expression was affected over the course of their illness.

They found that the virus inhibited genes that produce proteins used in energy production, forcing cells to use an alternative approach, which the virus also hijacked to make more copies of itself. This disruption was detected in multiple organs, including the lungs, heart, liver and kidneys. Examining tissue from patients who had died after catching COVID-19, they found that while mitochondrial function had recovered in their lungs, it remained suppressed in their heart, liver and kidneys.

Further studies in mice and hamsters infected with SARS-CoV-2 largely mirrored these findings, but also identified shifts in cellular metabolism within brain cells.

“This study provides us with strong evidence that we need to stop looking at COVID-19 as strictly an upper respiratory disease and start viewing it as a systemic disorder that impacts multiple organs,” said Wallace. “The continued dysfunction we observed in organs other than the lungs suggests that mitochondrial dysfunction could be causing long-term damage to the internal organs of these patients.”

While further studies are needed to confirm this in people with Long COVID, the team speculated that therapies targeting mitochondrial function might reduce COVID-19 symptoms, both during the early stages of infection and in patients living with chronic disease.