The lungs were once at the forefront of SARS-Cov-2 research, but as reports of organ failure and other serious complications poured in, scientists set out to discover how and why the respiratory virus was causing serious damage to the body’s major organs, including the lungs.
An interdisciplinary COVID-19 International Research Team (COV-IRT), which includes UNC School of Medicine’s Jonathan C. Schisler, PhD, found that SARS-CoV-2 alters mitochondria on a genetic level, leading to widespread “energy outages” throughout the body and its major organs. Their findings, published in Science Translational Medicine, explain how these effects contribute to long COVID symptoms and point to new therapeutic targets.
“We found that at peak infection time, there are distinct changes in different regions of the brain, including is a large decrease in mitochondrial genes in the cerebellum, the part of the brain that controls our muscles, balance, cognition, and emotion” said Schisler, assistant professor of pharmacology and member of the UNC McAllister Heart Institute. “The lung is the primary site of infection, but molecular signals are being transmitted affecting the entire body, with the heart, kidney, and liver being more affected than others, even long after the virus is gone.”
Every cell in our bodies is equipped with biological power stations known as mitochondria, which are especially important for maintaining the function of energy-demanding organs, such as the heart, brain, and lungs. Mitochondria require genes from their own genome (mitochondrial DNA) and nuclear DNA (nDNA) to create energy. Together, they instruct the mitochondria to convert oxygen molecules into cellular energy called adenosine triphosphate (ATP).