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<p>Viral myocarditis (VMC), caused by pathogens such as coxsackievirus B3 (CVB3), leads to severe cardiac injury and currently lacks specific therapeutic options. Here, we report a biomimetic antiviral strategy based on receptor engineering and intracellular gelation. By combining genetic and protein engineering, we generated a high-affinity Coxsackievirus and adenovirus receptor mutant (Mut-1_CAR) that markedly enhances the binding of host cardiomyocytes to CVB3. Using photochemical crosslinking, these engineered cells were converted into structurally stable, function-retaining gelated cells (PMs). PMs efficiently adsorb and neutralize virus particles, significantly reducing CVB3 plaque formation in vitro. In a murine model of viral myocarditis, PMs demonstrated excellent in vivo safety and biocompatibility while effectively lowering viral load and mitigating myocardial injury. This study establishes a “receptor enhancement + function fixation” approach for non-immune-dependent viral neutralization, providing a conceptual and technical foundation for the development of novel cell-based biomimetic antiviral therapies.</p> Graphical Abstract <p></p>

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Combining receptor engineering and intracellular gelation for cell-based antiviral therapy against coxsackievirus B3

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月17日

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  • Tonggong Liu,
  • Wenjuan Liu,
  • Ziyuan Peng,
  • Jie Wen,
  • Shengjie Wu,
  • Xiaona Zhao,
  • Jingzhe Wang,
  • Dayong Gu

摘要

Viral myocarditis (VMC), caused by pathogens such as coxsackievirus B3 (CVB3), leads to severe cardiac injury and currently lacks specific therapeutic options. Here, we report a biomimetic antiviral strategy based on receptor engineering and intracellular gelation. By combining genetic and protein engineering, we generated a high-affinity Coxsackievirus and adenovirus receptor mutant (Mut-1_CAR) that markedly enhances the binding of host cardiomyocytes to CVB3. Using photochemical crosslinking, these engineered cells were converted into structurally stable, function-retaining gelated cells (PMs). PMs efficiently adsorb and neutralize virus particles, significantly reducing CVB3 plaque formation in vitro. In a murine model of viral myocarditis, PMs demonstrated excellent in vivo safety and biocompatibility while effectively lowering viral load and mitigating myocardial injury. This study establishes a “receptor enhancement + function fixation” approach for non-immune-dependent viral neutralization, providing a conceptual and technical foundation for the development of novel cell-based biomimetic antiviral therapies.

Graphical Abstract