ITGB4/CD104 mediates zika virus attachment and infection

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.

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Publication Details

Journal
Nature Communications
Published
2024-12-30
DOI
https://doi.org/10.1038/s41467-024-54479-5
Citations
4
Primary Topic
Mosquito-borne diseases and control
Type
article
Field-Weighted Citation Impact
2.17

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article

ITGB4/CD104 mediates zika virus attachment and infection

Lei Song, Xiaodong Han, Shuifang Zhu, Tie-Shan Tang et al.
4 citations
Nature Communications
Mosquito-borne diseases and control
2.17
article

ITGB4/CD104 mediates zika virus attachment and infection

Lei Song, Xiaodong Han, Shuifang Zhu, Tie-Shan Tang, Jiuqiang Wang, Chang‐Mei Liu, Yang Yang, Ruigang Wang, Ning Du, Rong Lei, Haolong Cong
article en
4 citations

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.

Nature CommunicationsVol. 15(1)
Inner Mongolia Agricultural University (CN), Binzhou Medical University (CN), Shandong University of Aeronautics (CN), Chinese Academy of Sciences (CN), Inner Mongolia University (CN), Sinovac Biotech (CN), Institute for Stem Cell Biology and Regenerative Medicine (IN), Chinese Academy of Inspection and Quarantine (CN), Wuhan Institute of Virology (CN), University of Chinese Academy of Sciences (CN), Institute of Zoology (CN)
National Natural Science Foundation of China, Natural Science Foundation of Inner Mongolia
Openalex Percentile: Top 11%
Mosquito-borne diseases and control
2.17
DOIOpen Access PDFOpenAlex
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