ITGB4/CD104 mediates zika virus attachment and infection

Haolong Cong, Jiuqiang Wang, Ning Du, Lei Song, Ruigang Wang, Yang Yang, Rong Lei, Tie-Shan Tang (), Chang-Mei Liu (), Shuifang Zhu () and Xiaodong Han ()
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Haolong Cong: Chinese Academy of Inspection and Quarantine
Jiuqiang Wang: Binzhou Medical University
Ning Du: Chinese Academy of Sciences
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
Chang-Mei Liu: University of Chinese Academy of Sciences
Shuifang Zhu: Chinese Academy of Inspection and Quarantine
Xiaodong Han: Inner Mongolia Agriculture University

Nature Communications, 2024, vol. 15, issue 1, 1-12

Abstract: 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.

Date: 2024
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DOI: 10.1038/s41467-024-54479-5

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