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Myeloid-associated differentiation marker is an essential host factor for human parechovirus PeV-A3 entry

Author

Listed:
  • Kanako Watanabe

    (Niigata University Graduate School of Health Sciences)

  • Tomoichiro Oka

    (National Institute of Infectious Diseases)

  • Hirotaka Takagi

    (National Institute of Infectious Diseases)

  • Sergei Anisimov

    (Niigata University Graduate School of Medical and Dental Sciences)

  • Shun-ichi Yamashita

    (Niigata University Graduate School of Medical and Dental Sciences)

  • Yoshinori Katsuragi

    (Niigata College of Nursing)

  • Masahiko Takahashi

    (Niigata University Graduate School of Medical and Dental Sciences)

  • Masaya Higuchi

    (Kanazawa Medical University School of Medicine)

  • Tomotake Kanki

    (Niigata University Graduate School of Medical and Dental Sciences)

  • Akihiko Saitoh

    (Niigata University Graduate School of Medical and Dental Sciences)

  • Masahiro Fujii

    (Niigata University Graduate School of Medical and Dental Sciences)

Abstract

Human parechovirus (PeV-A) is an RNA virus that belongs to the family Picornaviridae and it is currently classified into 19 genotypes. PeV-As usually cause mild illness in children and adults. Among the genotypes, PeV-A3 can cause severe diseases in neonates and young infants, resulting in neurological sequelae and death. In this study, we identify the human myeloid-associated differentiation marker (MYADM) as an essential host factor for the entry of six PeV-As (PeV-A1 to PeV-A6), including PeV-A3. The infection of six PeV-As (PeV-A1 to PeV-A6) to human cells is abolished by knocking out the expression of MYADM. Hamster BHK-21 cells are resistant to PeV-A infection, but the expression of human MYADM in BHK-21 confers PeV-A infection and viral production. Furthermore, VP0 capsid protein of PeV-A3 interacts with one extracellular domain of human MYADM on the cell membrane of BHK-21. The identification of MYADM as an essential entry factor for PeV-As infection is expected to advance our understanding of the pathogenesis of PeV-As.

Suggested Citation

  • Kanako Watanabe & Tomoichiro Oka & Hirotaka Takagi & Sergei Anisimov & Shun-ichi Yamashita & Yoshinori Katsuragi & Masahiko Takahashi & Masaya Higuchi & Tomotake Kanki & Akihiko Saitoh & Masahiro Fuji, 2023. "Myeloid-associated differentiation marker is an essential host factor for human parechovirus PeV-A3 entry," Nature Communications, Nature, vol. 14(1), pages 1-14, December.
  • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-37399-8
    DOI: 10.1038/s41467-023-37399-8
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    Cited by:

    1. Pamela E. Capendale & Inés García-Rodríguez & Anoop T. Ambikan & Lance A. Mulder & Josse A. Depla & Eline Freeze & Gerrit Koen & Carlemi Calitz & Vikas Sood & Renata Vieira de Sá & Ujjwal Neogi & Dasj, 2024. "Parechovirus infection in human brain organoids: host innate inflammatory response and not neuro-infectivity correlates to neurologic disease," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    2. Wenjie Qiao & Christopher M. Richards & Youlim Kim & James R. Zengel & Siyuan Ding & Harry B. Greenberg & Jan E. Carette, 2024. "MYADM binds human parechovirus 1 and is essential for viral entry," Nature Communications, Nature, vol. 15(1), pages 1-14, December.

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