Fierce Biotech Scientists and clinicians studying COVID-19 have long suspected that the disease doesn’t just affect the lungs, but many other organ systems too. Now, researchers have identified a mechanism that could explain why and reveal new pathways to find treatments for long COVID.
In a study published Aug. 9 in Science, a team led by Children’s Hospital of Philadelphia (CHOP) and the COVID-19 International Research Team (COV-IRT) presented data from experiments on human tissue samples and animal models showing that SARS-CoV-2 suppresses the genes in mitochondria, a component of cells that generates the energy they need to function. The changes were found throughout the lungs, brain, heart, kidneys, liver and lymph nodes during the acute stages of infection, and in some organs remained even after the virus itself had been cleared.
“This is a very important study,” Eric Topol, M.D., a cardiologist at Scripps Research Institute who was not affiliated with the investigation, told Fierce Biotech Research in an interview. “We haven’t really understood how important the mitochondria might be for long COVID, and this study is really elegant.” While this isn’t the first study to show that SARS-CoV-2 affects mitochondria, it is the first to show how the virus impacts their genes. Previous research had indicated that the virus’ presence is associated with a decline in oxidative phosphorylation, or OXPHOS, proteins, which drive energy-producing pathways in mitochondria. The new findings show that this is because the virus actively prevents OXPHOS genes from being transcribed.