Key result
ICAM-1 mediates EMCV entry, with ICAM-4 acting as a compensatory receptor in ICAM-1 deficiency.
Why the study?
The receptors required for encephalomyocarditis virus (EMCV) entry into cells were unknown despite its widespread impact on piglet mortality.
ICAM-1 and ICAM-4 are identified as functional entry receptors for encephalomyocarditis virus, highlighting ICAM-1 domain 1 as a potential antiviral target.
Encephalomyocarditis virus (EMCV) is the most widespread zoonotic pathogen that causes piglet death. EMCV enters cells via caveolin-mediated endocytosis. However, the receptors required for EMCV entry into the cells are unknown. Here, we show that intercellular cell adhesion molecule-1 (ICAM-1) serves as a significant functional receptor during adsorption and entry. ICAM-1 binds directly to the EMCV viral proteins VP1 and VP2 with high affinity. Consistently, a soluble ICAM-1 fusion protein or anti-ICAM-1 blocking antibody impairs EMCV infection in susceptible human and mouse cells. Domain 1 of ICAM-1 is involved in the recognition of EMCV. ICAM-4 serves as a receptor in ICAM-1 knockout/knockdown mice and cell lines during EMCV infection. These findings suggest that ICAM-1 and ICAM-4 are entry receptors for EMCV and that targeting ICAM-1 D1 could be a potential strategy for the development of antivirals against EMCV.
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Hou et al. (2026) studied Encephalomyocarditis virus (EMCV) infection. ICAM-1 knockout or blocking (soluble ICAM-1 fusion protein / anti-ICAM-1 blocking antibody) vs. Control cells or wild-type mice was evaluated on EMCV infection, adsorption, and entry. ICAM-1 serves as a functional receptor for EMCV entry, and ICAM-4 functions as a compensatory receptor in ICAM-1 knockout models.
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