University of Minnesota Researchers Identify Structural Mechanisms Driving High Lethality of Marburg Virus

University of Minnesota scientists find Marburg virus enters cells 300x faster than Ebola, identifying a key vulnerability for new antivirals.

By: AXL Media

Published: Mar 13, 2026, 7:30 AM EDT

Source: Information for this report was sourced from University of Minnesota Medical School

University of Minnesota Researchers Identify Structural Mechanisms Driving High Lethality of Marburg Virus - article image
University of Minnesota Researchers Identify Structural Mechanisms Driving High Lethality of Marburg Virus - article image

Molecular Efficiency Uncovered in World’s Deadliest Pathogen

Researchers at the University of Minnesota Medical School have published a definitive study in the journal Nature exploring the hyper-efficient entry mechanisms of the Marburg virus. With an average fatality rate of 73 percent, Marburg has long been recognized as one of the most lethal pathogens in existence. The new data demonstrates that the virus possesses an unusual capacity to invade human cells, far surpassing the efficiency of its close relative, Ebola. By designing a tightly controlled comparison system, the research team was able to quantify that Marburg's entry protein drives infection at a rate significantly higher than previously understood, providing a biological explanation for its high mortality.

Structural Divergence Between Marburg and Ebola Entry Proteins

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The study highlights critical differences in how filoviruses interact with human biological receptors. While both Marburg and Ebola utilize the same human receptor for cellular entry, the Marburg virus employs its entry protein in a distinct orientation. According to the research led by Dr. Fang Li, professor of pharmacology, the Marburg protein exhibits a much higher affinity for the receptor than its counterparts. This increased binding strength, combined with a unique ability to change shape during the infection process, facilitates a rapid and aggressive entry into the host cell, which may account for the swift progression of the disease in clinical cases.

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