Author Interviews, Infections / 24.08.2025
Hebrew University Study Finds Fungus Contains Mycovirus That Makes Infections More Virulent and Difficult to Treat
MedicalResearch.com Interview with:
[caption id="attachment_70374" align="alignleft" width="200"]
Dr. Neta Shlezinger | Credit: Zuckerman Faculty Scholar Zuckerman Institute[/caption]
Dr. Neta Shlezinger Ph.D.
Koret School of Veterinary Medicine
Hebrew University
with Dr. Marina Campos Rocha Ph.D., Dr. Vanda Lerer, PhD., and student John Adeoye
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Fungal pathogens pose a growing threat to global health, particularly for immunocompromised individuals. Today, we appreciate that fungi kill more people each year than malaria and tuberculosis combined. Aspergillus fumigatus stands out as a leading cause of invasive fungal infections, responsible for approximately 65% of all invasive mold infections in humans.
These infections carry mortality rates that can exceed 50%, even with standard care. Treatment options remain limited: only a handful of antifungal drug classes are clinically available, and resistance is increasingly reported to all of them. As a result, the search for novel therapeutic strategies is now focused on fungal-specific virulence factors — targets that are essential for fungal survival and pathogenicity in the host but are absent in humans.
Meanwhile, research in recent years has revealed that many fungi harbor viruses. These mycoviruses are surprisingly prevalent, but their impact on fungal physiology and, crucially, on fungal pathogenicity in humans has remained largely unexplored.
Our study set out to fill this gap by examining a double-stranded RNA virus, Aspergillus fumigatus polymycovirus 1 (AfuPmV-1M), that naturally infects A. fumigatus. We found that this virus isn’t just a silent passenger — it’s wired into key fungal stress response pathways, helping the fungus survive heat stress, evade oxidative damage, and persist in the lung environment. In other words, it acts like a backseat driver — quietly steering the fungus toward enhanced survival and virulence.
When we “cured” the fungus of its virus, it produced fewer spores, made less melanin, became more vulnerable to stress, and caused milder infections in mice. Seeing this, we explored a therapeutic twist: fight the virus to clear the fungus.
We treated infected mice with antiviral compounds during fungal infection and observed reduced mycovirus levels and improved survival.
Together, these results suggest that mycoviruses can be overlooked drivers of fungal disease — and targeting them may represent a novel, host-sparing therapeutic strategy.
Dr. Neta Shlezinger | Credit: Zuckerman Faculty Scholar Zuckerman Institute[/caption]
Dr. Neta Shlezinger Ph.D.
Koret School of Veterinary Medicine
Hebrew University
with Dr. Marina Campos Rocha Ph.D., Dr. Vanda Lerer, PhD., and student John Adeoye
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Fungal pathogens pose a growing threat to global health, particularly for immunocompromised individuals. Today, we appreciate that fungi kill more people each year than malaria and tuberculosis combined. Aspergillus fumigatus stands out as a leading cause of invasive fungal infections, responsible for approximately 65% of all invasive mold infections in humans.
These infections carry mortality rates that can exceed 50%, even with standard care. Treatment options remain limited: only a handful of antifungal drug classes are clinically available, and resistance is increasingly reported to all of them. As a result, the search for novel therapeutic strategies is now focused on fungal-specific virulence factors — targets that are essential for fungal survival and pathogenicity in the host but are absent in humans.
Meanwhile, research in recent years has revealed that many fungi harbor viruses. These mycoviruses are surprisingly prevalent, but their impact on fungal physiology and, crucially, on fungal pathogenicity in humans has remained largely unexplored.
Our study set out to fill this gap by examining a double-stranded RNA virus, Aspergillus fumigatus polymycovirus 1 (AfuPmV-1M), that naturally infects A. fumigatus. We found that this virus isn’t just a silent passenger — it’s wired into key fungal stress response pathways, helping the fungus survive heat stress, evade oxidative damage, and persist in the lung environment. In other words, it acts like a backseat driver — quietly steering the fungus toward enhanced survival and virulence.
When we “cured” the fungus of its virus, it produced fewer spores, made less melanin, became more vulnerable to stress, and caused milder infections in mice. Seeing this, we explored a therapeutic twist: fight the virus to clear the fungus.
We treated infected mice with antiviral compounds during fungal infection and observed reduced mycovirus levels and improved survival.
Together, these results suggest that mycoviruses can be overlooked drivers of fungal disease — and targeting them may represent a novel, host-sparing therapeutic strategy.
