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在SARS-CoV-2尖端蛋白的多基分裂部位的序列糖基化调节病毒活性

Shengjun Wang1,2, Wei Ran3, Lingyu Sun1

  • 1School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.

Nature communications
|May 16, 2024
PubMed
概括

由GalNAc-T3和T7启动的宿主细胞糖化,抑制了SARS-CoV-2尖端蛋白处理和病毒感染. 病毒变种进化了对这种宿主防御机制的耐药性和易感性.

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