Study Finds Albumin Protects Against a Deadly Fungal Infection

A study published in Nature has revealed that albumin, the most abundant protein in human blood, plays an important role in defending the body against mucormycosis, a rare but often fatal fungal infection. The international research team was led by George Chamilos from the University of Crete and Institute of Molecular Biology and Biotechnology, with major contributions from Professor Ashraf Ibrahim and his team at The Lundquist Institute for Biomedical Innovation. 

Mucormycosis, sometimes known as “black fungus,” progresses rapidly and can be fatal in up to half of those affected. In some cases, diagnosis indicates a virtually certain outcome of death. The disease is caused by fungi belonging to the Mucorales group and surged in India during the COVID-19 pandemic, particularly among patients with diabetes, weakened immune systems, or malnutrition. 

The study found that patients with mucormycosis consistently exhibited lower levels of albumin than those with other fungal infections. This condition, called hypoalbuminemia, was the strongest predictor of severe outcomes, including death, among different populations across multiple continents. According to Dr. Ibrahim, “This is a remarkable finding and has the potential to change the way clinicians care for mucormycosis.” The results indicate that hypoalbuminemia may serve as a biomarker for identifying individuals at risk. In such cases, patients could receive albumin loaded with free fatty acids to prevent infection before it develops, offering a targeted approach to managing this aggressive disease.

“The study also tells us how albumin works on nullifying critical virulence factors including toxins and other fungal proteins involved in causing tissue damage and in aggressively invading human organs,” explained Dr. Ibrahim.  

The researchers demonstrated that albumin selectively inhibits Mucorales fungi while leaving other microbes unaffected. When albumin was removed from healthy blood samples, fungal growth increased significantly. Mice lacking albumin were highly susceptible to infection, while restoring albumin levels prevented disease. Further experiments showed that the protective effect stems from fatty acids bound to albumin, which disrupt fungal metabolism and block the production of proteins needed for tissue invasion. In patients, these fatty acids were found to be more heavily oxidized, possibly contributing to infection vulnerability.