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Aspergillus fumigatus dsRNA virus promotes fungal fitness and pathogenicity in the mammalian host

Summary

Researchers discovered that a virus infecting the dangerous fungus Aspergillus fumigatus actually helps the fungus survive and cause worse infections in humans. By removing the virus from fungal strains, scientists found that the fungus became weaker and less able to cause disease in mice. Importantly, treating infected mice with an antiviral drug (ribavirin) reduced the viral load and helped the mice survive, suggesting a new approach to treating serious fungal infections.

Background

Aspergillus fumigatus is responsible for approximately 65% of invasive fungal infections in humans with mortality rates approaching 50%. Mycoviruses, which are viruses that infect fungi, are prevalent in the fungal kingdom but their impact on fungal pathogenesis in mammals remains largely unexplored. This study investigates how a double-stranded RNA mycovirus affects fungal fitness and virulence.

Objective

To determine whether A. fumigatus polymycovirus-1M (AfuPmV-1M) enhances fungal fitness, stress tolerance, and pathogenicity in the mammalian host. The researchers compared virus-infected, virus-cured, and re-infected fungal strains to isolate viral effects on fungal virulence and disease progression.

Results

AfuPmV-1M enhanced conidiation, melanin production, and survival under oxidative, heat, and pH stress. The virus upregulated stress-granule components, RNA metabolism proteins, and antioxidants. Virus-infected strains showed increased survival in neutrophils and higher virulence in immunocompetent and immunocompromised mice. Ribavirin treatment reduced viral load and improved mouse survival.

Conclusion

AfuPmV-1M acts as a ‘molecular backseat driver’ promoting A. fumigatus fitness and pathogenicity through enhanced stress tolerance and conidiation. Antiviral treatment targeting mycoviral replication presents a novel therapeutic strategy for aspergillosis, suggesting mycoviruses are underappreciated modulators of fungal disease progression.
  • Published in:Nature Microbiology,
  • Study Type:Experimental Research,
  • Source: PMID: 40813922, DOI: 10.1038/s41564-025-02096-3
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