Scientists find key trigger of long COVID

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New research has identified a potential key factor in the development of long COVID: problems with iron regulation and inflammation due to SARS-CoV-2 infection.

This discovery, made by scientists from the University of Cambridge and Oxford, offers insight into not only potential treatments and prevention strategies for long COVID but also sheds light on why similar symptoms are observed in various post-viral conditions and chronic inflammatory diseases.

Long COVID, affecting as many as 30% of those infected with SARS-CoV-2, manifests in symptoms like persistent fatigue, breathing difficulties, muscle pains, and cognitive issues such as memory and concentration problems, commonly referred to as ‘brain fog’.

In the UK alone, around 1.9 million people were reported to be suffering from long COVID as of March 2023.

Researchers embarked on this study early in the pandemic, enrolling individuals who tested positive for COVID-19—from asymptomatic healthcare workers to severely ill patients in intensive care.

Over a year, they collected blood samples to monitor changes post-infection, enabling them to identify markers associated with the development of long COVID.

Their findings, published in Nature Immunology, reveal that inflammation and altered iron metabolism, noticeable as early as two weeks after infection, are linked to long COVID symptoms months later.

This disruption in iron levels and regulation was observed regardless of the initial severity of the COVID-19 infection, age, or sex, indicating that even those at lower risk for severe illness could face prolonged recovery issues due to these imbalances.

The research highlights how ongoing inflammation and iron dysregulation can impair the body’s ability to produce healthy red blood cells, impacting oxygen transport and energy production.

Interestingly, even though severe COVID-19 cases showed more significant iron dysregulation, individuals with milder infections experienced similar patterns if they developed long COVID, suggesting that the key issue is the duration it takes for inflammation and iron levels to normalize post-infection.

Iron dysregulation, a common response to inflammation and infection, serves as a protective mechanism by withholding iron from the bloodstream to limit bacterial growth.

However, prolonged dysregulation can lead to inefficiencies in oxygen transport and immune function, contributing to the fatigue and exercise intolerance seen in long COVID and other post-viral syndromes.

The study suggests that early interventions to manage inflammation or innovative strategies to correct iron distribution could mitigate long COVID’s impact.

While iron supplementation might seem an obvious solution, the challenge lies in remobilizing iron effectively back into the bloodstream rather than simply increasing the body’s iron supply.

This research not only contributes to our understanding of long COVID but also aligns with findings from other studies, such as the IRONMAN trial and observations in patients with beta-thalassemia, further emphasizing the complex relationship between iron metabolism, inflammation, and viral infections.

If you care about COVID, please read studies about Vitamin D deficiency linked to severe COVID-19, and how diets could help manage post-COVID syndrome.

For more information about COVID, please see recent studies about new evidence on rare blood clots after COVID-19 vaccination, and results showing zinc could help reduce COVID-19 infection risk.

The research findings can be found in Nature Immunology.

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