A Novel Virus Alters Gene Expression and Vacuolar Morphology in Malassezia Cells and Induces a TLR3-Mediated Inflammatory Immune Response

Author:

Park Minji1,Cho Yong-Joon2,Kim Donggyu3,Yang Chul-Su34,Lee Shi Mun56,Dawson Thomas L.57689,Nakamizo Satoshi56,Kabashima Kenji5106,Lee Yang Won1112,Jung Won Hee1ORCID

Affiliation:

1. Department of Systems Biotechnology, Chung-Ang University, Anseong, South Korea

2. The Research Institute of Basic Sciences, Seoul National University, Seoul, South Korea

3. Department of Molecular and Life Science, Hanyang University, Ansan, South Korea

4. Department of Bionano Technology, Hanyang University, Seoul, South Korea

5. Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Biopolis, Singapore

6. Skin Research Institute of Singapore (SRIS), Agency for Science, Technology and Research (A*STAR), Biopolis, Singapore

7. Center for Cell Death, Injury & Regeneration, Medical University of South Carolina, Charleston, South Carolina, USA

8. Department of Drug Discovery & Biomedical Sciences, Medical University of South Carolina, Charleston, South Carolina, USA

9. Department of Biochemistry & Molecular Biology, Medical University of South Carolina, Charleston, South Carolina, USA

10. Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan

11. Department of Dermatology, School of Medicine, Konkuk University, Seoul, South Korea

12. Research Institute of Medicine, Konkuk University, Seoul, South Korea

Abstract

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, Malassezia 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 sequence and structure of the viral genome along with an independent satellite dsRNA viral segment. Moreover, expression of genes involved in ribosomal synthesis and programmed cell death was altered, indicating that virus infection affected 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, indicating that a viral element likely contributes to the pathogenicity of Malassezia . This is the first study to identify and characterize a novel mycovirus in Malassezia .

Funder

National Research Foundation of Korea

Publisher

American Society for Microbiology

Subject

Virology,Microbiology

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