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ITGB4/CD104 mediates zika virus attachment and infection

Author

Listed:
  • Haolong Cong

    (Chinese Academy of Inspection and Quarantine
    Chinese Academy of Sciences)

  • Jiuqiang Wang

    (Binzhou Medical University
    Chinese Academy of Sciences)

  • Ning Du

    (Chinese Academy of Sciences
    Ltd.)

  • Lei Song

    (Chinese Academy of Sciences)

  • Ruigang Wang

    (Inner Mongolia Agriculture University)

  • Yang Yang

    (Chinese Academy of Sciences)

  • Rong Lei

    (Chinese Academy of Inspection and Quarantine)

  • Tie-Shan Tang

    (Chinese Academy of Sciences
    University of Chinese Academy of Sciences
    Chinese Academy of Sciences
    Beijing Institute for Stem Cell and Regenerative Medicine)

  • Chang-Mei Liu

    (University of Chinese Academy of Sciences
    Chinese Academy of Sciences
    Beijing Institute for Stem Cell and Regenerative Medicine
    Chinese Academy of Sciences)

  • Shuifang Zhu

    (Chinese Academy of Inspection and Quarantine)

  • Xiaodong Han

    (Inner Mongolia Agriculture University)

Abstract

Zika virus (ZIKV) infection can result in a birth defect of the brain called microcephaly and other severe fetal brain defects. ZIKV enters the susceptible host cells by endocytosis, which is mediated by the interaction of the envelope (E) glycoprotein with cellular surface receptor molecules. However, the cellular factors that used by the ZIKV to gain access to host cells remains elusive. Here, we report that the extracellular domain of integrin beta 4 (ITGB4) is an entry factor of ZIKV. ITGB4 mediates ZIKV infection by directly interacting with the E glycoprotein of ZIKV, and ITGB4 knockout hampers the binding and replication of ZIKV to host cells. A functional monoclonal antibody against ITGB4 or the soluble forms of ITGB4 could decrease the binding and infection of ZIKV to permissive cell lines. Importantly, the ITGB4 antibody blocks the infection of ZIKV to mouse placenta, thus protecting the fetuses from ZIKV infection. Together, our study has demonstrated that ZIKV infection involves ITGB4 dependent binding.

Suggested Citation

  • Haolong Cong & Jiuqiang Wang & Ning Du & Lei Song & Ruigang Wang & Yang Yang & Rong Lei & Tie-Shan Tang & Chang-Mei Liu & Shuifang Zhu & Xiaodong Han, 2024. "ITGB4/CD104 mediates zika virus attachment and infection," Nature Communications, Nature, vol. 15(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-54479-5
    DOI: 10.1038/s41467-024-54479-5
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    References listed on IDEAS

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    1. Fernanda R. Cugola & Isabella R. Fernandes & Fabiele B. Russo & Beatriz C. Freitas & João L. M. Dias & Katia P. Guimarães & Cecília Benazzato & Nathalia Almeida & Graciela C. Pignatari & Sarah Romero , 2016. "The Brazilian Zika virus strain causes birth defects in experimental models," Nature, Nature, vol. 534(7606), pages 267-271, June.
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