Enterovirus 71 (EV71) was the major causative agent of hand, foot, and mouth disease, resulting in serious complications in children. It was worth noting that viruses must be provided with energy and raw materials for synthesis by hijacking the host cell metabolism. Lacto--fucopentaose I (LNFPI), as one of representative oligosaccharide in human milk, had been demonstrated to inhibit the EV71 infection. However, the regulatory mechanisms of LNFPI for metabolic changes caused by EV71 remained largely unknown. This work aimed to reveal the regulatory effects of LNFPI on metabolic abnormalities induced by EV71. The results showed that LNFPI induced an increase in the expression of glucose-6-phosphate transporter by down-regulating GLUT2, thereby reducing energy hijacking and alleviating metabolic abnormalities caused by EV71 infection. This intervention also hindered the transcription and metabolism of nucleotides, consequently inhibiting EV71 replication.

中文翻译：

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岩藻糖基化寡糖乳-N-岩藻五糖 I 通过抑制异常糖酵解减轻肠道病毒 71 感染的症状


肠道病毒71型（EV71）是手足口病的主要病原体，可导致儿童出现严重并发症。值得注意的是，病毒必须通过劫持宿主细胞代谢来提供合成所需的能量和原料。乳岩藻糖五糖 I (LNFPI) 作为人乳中代表性的低聚糖之一，已被证明具有抑制 EV71 感染的作用。然而，LNFPI 对 EV71 引起的代谢变化的调节机制仍不清楚。本工作旨在揭示LNFPI对EV71引起的代谢异常的调节作用。结果表明，LNFPI通过下调GLUT2诱导葡萄糖-6-磷酸转运蛋白表达增加，从而减少能量劫持，缓解EV71感染引起的代谢异常。这种干预还阻碍了核苷酸的转录和代谢，从而抑制了 EV71 的复制。