在登革热病毒2感染的肝细胞中,糖解降低
Chanida Chumchanchira1,2, Suwipa Ramphan2, Wannapa Sornjai2
1PhD Degree Program in Biology (International Program), Faculty of Science, Chiang Mai University, Chiang Mai, 50200, Thailand.
Scientific reports
|April 9, 2024
概括
肝细胞中的登革热病毒 (DENV) 感染会降低葡萄糖分解的调节,影响细胞代谢. 抗糖尿病药物梅特福林减少了DENV感染,表明了治疗潜力.
科学领域:
- * 病毒学 病毒学
- * 细胞生物学 细胞生物学
- * 蛋白质组学 蛋白质组学
背景情况:
- *登革热病毒 (DENV) 感染对全球健康构成重大挑战.
- *肝细胞是已知的点,但DENV感染期间的蛋白质组变化尚未得到充分研究.
- *了解细胞反应对于开发抗病毒策略至关重要.
研究的目的:
- * 在DENV-2感染后调查肝细胞中的蛋白质组变化.
- * 为了识别DENV-2调节的关键细胞蛋白.
- * 探索糖解的作用和潜在的治疗干预措施.
主要方法:
- *二维凝电泳 (2D-PAGE) 用于在感染后12小时和48小时 (hpi) 对感染的Hep3B细胞进行蛋白质组分析.
- * 西方涂抹用于验证Hep3B和iPSC衍生肝细胞中的甘甲基-3-酸盐脱酶 (GAPDH) 表达.
- *测量NAD+/NADH比率并评估甲胺对DENV-2感染的影响.
主要成果:
- *确定了4个在12hpi和14个在48hpi的不同表达的蛋白质.
- *确认了GAPDH的下调,导致NADH增加和NAD+/NADH比率降低,表明糖解抑制.
- * 甲胺治疗降低了DENV-2感染水平和病毒产量.
结论:
- * DENV-2 感染降低肝细胞中的葡萄糖分解.
- *尽管降低了糖解,但葡萄糖是必不可少的,可能是支持病毒复制的酸通路.
- * 甲胺显示出降低DENV-2感染的潜力,需要进一步调查.
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