New research has identified damage to mitochondria, the cellular “power plants,” as a crucial factor in the development of severe COVID-19, providing new insights into how the virus triggers widespread organ and immune system dysfunction. The findings, published Nov. 27 in the Proceedings of the National Academy of Sciences, shed light on the complex molecular mechanisms behind the disease’s deadliest symptoms.
Led by scientists from Weill Cornell Medicine, Johns Hopkins Medicine, the Children’s Hospital of Philadelphia, and the University of Pittsburgh, the study examined tissue samples from patients and animal models to uncover how SARS-CoV-2, the virus that causes COVID-19, disrupts cellular function. Researchers observed that mitochondrial damage in infected cells activates the immune system, driving the excessive inflammatory response known as a “cytokine storm.”
This cascade, the study found, involves the overactivation of the renin-angiotensin-activation-system (RAAS), a blood-pressure-regulating mechanism. Overactive RAAS has been linked to severe COVID-19 symptoms, including abnormal blood clotting, scarring in lymph nodes, and impaired immune function.
“These findings suggest that early in the process, profound mitochondrial dysfunction is driving RAAS overactivation, contributing to the multi-organ damage seen in severe COVID-19,” said Dr. Robert Schwartz, associate professor of medicine at Weill Cornell Medicine and one of the study’s senior authors. Schwartz also warned of potential lingering effects, noting that these pathways may not fully resolve in some patients, potentially contributing to “long COVID.”
The research team used advanced techniques such as RNA sequencing to analyze de-identified patient samples, including nasopharyngeal swabs and organ tissues, as well as COVID-19 animal models provided by Weill Cornell Medicine. Their work highlights the intricate interplay between viral infection, mitochondrial damage, and immune overactivation.
The study also raises questions about the long-term impact of these mechanisms. Researchers are now investigating whether mitochondrial damage and immune dysfunction persist in cases of long COVID, a condition marked by chronic inflammation and ongoing health challenges.
The study was supported by the National Institute of Allergy and Infectious Diseases and the Department of Defense, underscoring its significance in advancing the understanding of COVID-19.
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