Nectin-4 mediates rubella virus entry in airway and placental cells.

Nectin-4 is identified as a functional rubella virus entry receptor, enabling infection in non-permissive cells and mediating basolateral entry in polarized airway epithelium.

• Why it matters: The cellular entry mechanism of rubella virus is poorly defined because host receptors are limited, slowing pathogenesis research and therapeutic development.
• What they did: Proximity biotin labelling-based proteomics plus CRISPR-Cas9 validation identified nectin-4, and ectopic expression, blocking, and genetic ablation tested its role; mechanistic assays showed direct interaction with the RuV envelope glycoprotein heterodimer and calcium-dependent attachment to lipids.
• The result: In polarized airway epithelial models, nectin-4 mediates basolateral entry and supports apical progeny release, while in placental models it is highly expressed on syncytiotrophoblasts and facilitates maternal-fetal interface infection.

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