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Related Experiment Videos

Q&A with Bin Cao.

Bin Cao

    Cell Reports
    |May 1, 2025
    PubMed
    Summary
    This summary is machine-generated.

    Hepatitis A virus cellular receptor 1 (HAVCR1) acts as a receptor for Zika virus entry into placental cells. This interaction is crucial for Zika virus vertical transmission from mother to fetus.

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    Area of Science:

    • Virology
    • Reproductive biology
    • Immunology

    Background:

    • Zika virus (ZIKV) poses a significant threat to pregnant women, causing severe fetal abnormalities.
    • The mechanisms underlying ZIKV placental infection and vertical transmission remain incompletely understood.
    • Identifying host factors involved in ZIKV entry is critical for developing therapeutic strategies.

    Purpose of the Study:

    • To investigate the role of Hepatitis A virus cellular receptor 1 (HAVCR1) in ZIKV infection of placental cells.
    • To determine if HAVCR1 mediates ZIKV entry into human placental trophoblasts.
    • To elucidate the contribution of HAVCR1 to ZIKV vertical transmission.

    Main Methods:

    • Utilized human placental trophoblast cell models.
    • Employed gene silencing techniques to downregulate HAVCR1 expression.

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  • Assessed ZIKV infection levels and viral particle production.
  • Analyzed the impact of HAVCR1 on placental barrier integrity.

    • Main Results:

    • HAVCR1 was identified as a functional receptor for ZIKV on human placental trophoblasts.
    • Downregulation of HAVCR1 significantly reduced ZIKV entry and replication in placental cells.
    • HAVCR1 expression in trophoblasts correlates with increased susceptibility to ZIKV infection.
    • HAVCR1-mediated ZIKV entry impacts placental barrier function, potentially facilitating vertical transmission.

    Conclusions:

    • HAVCR1 is a key host factor mediating ZIKV infection in the placenta.
    • Targeting HAVCR1 may represent a novel therapeutic approach to prevent ZIKV vertical transmission.
    • Further research is warranted to explore HAVCR1's precise role in the pathogenesis of congenital Zika syndrome.