Virus inside the fungus drives deadly fungal infections

Researchers have discovered that a virus living inside the fungus Aspergillus fumigatus significantly boosts the fungus's ability to survive stress and cause severe infections in mammals. Removing the virus made the fungus weaker and less virulent, while antiviral treatments improved survival outcomes. This finding reveals a hidden factor driving the deadliness of fungal infections and opens the door to potential new treatments that target the virus rather than the fungus itself.

A new study by researchers at The Hebrew University of Jerusalem in collaboration with researchers from the Institute of Microbiology at Friedrich Schiller University, has uncovered an unexpected culprit fueling the severity of one of the most dangerous fungal infections in humans: a virus living inside the fungus itself.

Led by Dr. Marina Campos Rocha, Dr. Vanda Lerer, PhD., and Student John Adeoye under the supervision of Dr. Neta Shlezinger of the Koret School of Veterinary Medicine at Hebrew University, the research reveals that a virus residing within the Aspergillus fumigatus fungus gives it a powerful survival advantage—making it tougher, more resilient, and ultimately, more dangerous to human health.

A hidden influence in a dangerous pathogen

Aspergillus fumigatus is already notorious in medical circles. Responsible for the majority of invasive fungal infections in humans, it's especially lethal for people with weakened immune systems. Despite decades of research, mortality rates from infections remain alarmingly high—approaching 50%.

But Dr. Shlezinger's team has added a surprising new layer to the story: a double-stranded RNA virus, quietly riding along inside the fungus, appears to act like a hidden booster pack for the pathogen. When this virus is present, the fungus becomes far more adept at surviving environmental stress, including the heat and oxidative conditions inside the lungs of mammals.

Virus-cured fungi lose their edge

To test the impact of the virus, the researchers removed it from fungal strains and compared their behavior to their virus-infected counterparts. The difference was striking. The virus-free fungi lost their ability to reproduce effectively, showed weaker defenses like reduced melanin production, and became significantly less dangerous when introduced into mammalian lungs.

The findings suggest that these so-called "mycoviruses" may play a quiet but critical role in the development and progression of fungal diseases in humans—a role that has largely gone unnoticed in the field of medical mycology.

Hope for new treatments

Perhaps most promising of all: when antiviral treatments were used to suppress the virus during infection, survival outcomes improved in the mammalian model. This hints at a whole new treatment avenue—not just targeting the fungus itself, but the virus helping it thrive.

"These viruses are like molecular backseat drivers," says Dr. Shlezinger. "They don't cause disease on their own, but they influence how aggressively the fungus behaves once it's inside the body."

A paradigm shift in fighting fungal infections

This discovery opens the door to rethinking how fungal infections are treated. By targeting the virus within the fungus, researchers may one day weaken the pathogen enough for the immune system—or existing antifungal drugs—to fight back more effectively.

In a world where fungal pathogens are becoming more drug-resistant and harder to treat, the study provides a rare glimmer of hope: perhaps we've been overlooking a key player all along.

Source:
Journal reference:

Rocha, M. C., et al. (2025). Aspergillus fumigatus dsRNA virus promotes fungal fitness and pathogenicity in the mammalian host. Nature Microbiology. doi.org/10.1038/s41564-025-02096-3.

Comments

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News Medical.
Post a new comment
Post

While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. We do not provide medical advice, if you search for medical information you must always consult a medical professional before acting on any information provided.

Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles.

Please do not ask questions that use sensitive or confidential information.

Read the full Terms & Conditions.

You might also like...
How cohesin mechanics and nanotracker tech are redefining DNA research