Researchers at the University of Virginia School of Medicine have found a potential treatment for the respiratory symptoms of long COVID by uncovering a previously unknown cause within the lungs.
The study, led by Jie Sun, Ph.D., revealed that COVID-19 can trigger significant changes in immune cells in lung tissues, leading to scarring and persistent inflammation even after the initial infection has subsided.
This ongoing inflammation is believed to cause the lasting respiratory symptoms, such as cough and difficulty breathing, seen in long COVID.
Sun and his team discovered that doctors might be able to stop this chronic inflammation using a class of drugs, including baricitinib, which are already used to treat rheumatoid arthritis.
These anti-inflammatory drugs had previously received emergency authorization from the FDA for treating the uncontrolled inflammation in severe COVID-19 cases. The findings were published in the journal Science Translational Medicine.
“Our study identified a root cause of the respiratory complications of long COVID by performing comparative analysis of both clinical samples and a relevant animal model,” said Sun, from UVA’s Carter Center for Immunology Research and UVA’s Division of Infectious Diseases and International Health.
“We hope that identifying the ‘driving’ mechanisms will help design clinical studies repurposing those FDA-approved drugs for respiratory long COVID soon.”
Long COVID affects over 60 million people worldwide, turning a COVID-19 infection into a prolonged ordeal with symptoms that can last weeks, months, or even years.
These symptoms range from uncomfortable to debilitating, including shortness of breath, chest pain, and chronic lung scarring known as interstitial lung disease.
While previous research into long COVID focused on patients’ blood, Sun and his team examined the lung tissues directly. They analyzed cell samples from the lower airways of both lab mice and human patients.
In both cases, they found that immune cells, specifically macrophages and T cells, were behaving abnormally and interacting harmfully. These cells, which usually help the body fight off disease, continued their activity long after the initial COVID infection had cleared.
The researchers discovered that macrophages had accumulated in large numbers in the lungs, promoting tissue scarring. Meanwhile, T cells were producing a substance called interferon, which caused ongoing inflammation.
Sun and his colleagues believe that drugs already approved for treating rheumatoid arthritis, which targets similar inflammatory pathways, could break this cycle of inflammation in long COVID patients.
Although further research is needed, Sun hopes that these new findings will lead to much-needed treatments for those suffering from long COVID’s respiratory symptoms.
“We hope our clinical colleagues around the globe could perform clinical trials soon to test the efficacy of baricitinib or other similar drugs targeting the same inflammatory pathway in long COVID,” Sun said.
“Our new study has established a foundation for identifying new therapeutic interventions for long COVID by combining rigorous clinical testing and basic scientific research.”
The research team included Chaofan Li, Wei Qian, Xiaoqin Wei, Harish Narasimhan, Yue Wu, Mohd Arish, In Su Cheon, Jinyi Tang, Gislane de Almeida Santos, Ying Li, Kamyar Sharifi, Ryan Kern, Robert Vassallo, and Sun.
If you care about COVID-19, please read studies about vitamin D deficiency linked to severe COVID-19, death, and how diets could help manage post-COVID syndrome.
For more information about health, please see recent studies about COVID infection and vaccination linked to heart disease, and results showing extracts from two wild plants can inhibit COVID-19 virus.
The research findings can be found in Science Translational Medicine.
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