Abstract
Most fungal viruses have been identified in plant pathogens, whereas the presence of viral particles in human pathogenic fungi is less well studied. In the present study, we observed extrachromosomal double-stranded RNA (dsRNA) segments in various clinical isolates of Malassezia species. Malassezia is the most dominant fungal genus on the human skin surface, and species in this group are considered to be etiological factors in various skin diseases including dandruff, seborrheic dermatitis, and atopic dermatitis. We identified novel dsRNA segments and our sequencing results revealed that the virus, named MrV40, belongs to the Totiviridae family and contains an additional satellite dsRNA segment encoding a novel protein. The transcriptome of virus-infected M. restricta cells was compared to that of virus-free cells, and the results showed that transcripts involved in ribosomal biosynthesis were down regulated and those involved in energy production and programmed cell death were increased in abundance. Moreover, transmission electron microscopy revealed significantly larger vacuoles for virus-infected M. restricta cells, indicating that MrV40 infection dramatically altered M. restricta physiology. Our analysis also revealed that a viral nucleic acid from MrV40 induces a TLR3-mediated inflammatory immune response in bone marrow-derived dendritic cells (BMDCs) and this result suggests that a viral element contributes to the pathogenesis of Malassezia.
Importance Malassezia is the most dominant fungal genus on the human skin surface and is associated with various skin diseases including dandruff and seborrheic dermatitis. Among Malassezia species, M. restricta is the most widely observed species on the human skin. In the current study, we identified a novel dsRNA virus, named MrV40, in M. restricta and characterized the sequences and structure of the viral genome along with an independent satellite dsRNA viral segment. Moreover, we found altered expression of genes involved in ribosomal synthesis and programmed cell death, indicating that virus infection altered the physiology of the fungal host cells. Our data also showed that the viral nucleic acid from MrV40 induces a TLR3-mediated inflammatory immune response in bone marrow-derived dendritic cells (BMDCs), indicating that a viral element likely contributes to the pathogenesis of Malassezia. This is the first study to identify and characterize a novel mycovirus in Malassezia.