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Updated: Jul 10, 2026

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
09:11

Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons

Published on: August 23, 2016

The HAVCR1-centric host factor network drives Zika virus vertical transmission

Wenzhe Yu1, Jun Tao1, Hongmin Cao1

  • 1Fujian Provincial Key Laboratory of Reproductive Health Research, the First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, Fujian, China.

Cell Reports
|March 29, 2025
PubMed

Zika virus (ZIKV) vertical transmission results in devastating congenital malformations and pregnancy complications; however, the specific receptor and host factors facilitating ZIKV maternal-fetal transmission remain elusive. Here, we employ a genome-wide CRISPR screening and identify multiple placenta-intrinsic factors modulating ZIKV infection. Our study unveils that hepatitis A virus cellular receptor 1 (HAVCR1) serves as a primary receptor governing ZIKV entry in placental trophoblasts. The GATA3-HAVCR1 axis regulates heterogeneous cell tropism in the placenta. Notably, placenta-specific Havcr1 deletion in mice significantly impairs ZIKV transplacental transmission and associated adverse pregnancy outcomes. Mechanistically, the immunoglobulin variable-like domain of HAVCR1 binds to ZIKV via domain III of envelope protein and virion-associated phosphatidylserine. Proteomic profiling and function analyses reveal that AP2S1 cooperates with HAVCR1 for ZIKV internalization through clathrin-mediated endocytosis. Overall, our work underscores the pivotal role of HAVCR1 in mediating ZIKV vertical transmission and highlights a therapeutic target for alleviating congenital Zika syndrome.

Keywords:
AP2S1CP: MicrobiologyGATA3HAVCR1IgV domainZIKV receptorclathrin-mediated endocytosisgenome-wide CRISPR screensplacental trophoblastsusceptibilityvertical transmission

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