细胞内膜网膜与压力相关的未折叠蛋白质反应的作用及其对登革热病毒感染对生物标志物发展的影响
Biswadeep Das1, Sagnika Samal1, Hamida Hamdi2
1School of Biotechnology, Kalinga Institute of Industrial Technology, KIIT Deemed to Be University, Bhubaneswar, Odisha 751024, India.
Life sciences
|July 30, 2023
概括
登革热病毒感染调高了未展开的蛋白质反应 (UPR),这是细胞应激途径,导致失调的自. 准UPR途径为新的登革热病毒疗法提供了潜力.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 登革热病毒 (DENV) 感染在不同的人类宿主细胞中表现出不同的速率.
- 影响DENV感染异质性的因素包括宿主免疫反应,抗病毒蛋白和病毒自.
- 展开的蛋白质反应 (UPR) 是一种细胞机制,可以抵消内质网膜 (ER) 压力.
研究的目的:
- 审查未折叠蛋白质反应 (UPR) 在登革热病毒 (DENV) 感染中的作用.
- 探索DENV如何调节UPR通路和细胞自.
- 确定UPR作为登革热感染的潜在治疗点.
主要方法:
- 审查关于DENV感染和UPR的现有文献.
- 在DENV的背景下对UPR信号通路 (IRE1,PERK,ATF6) 的分析.
- 检查调节自和亡的下游作用因子 (XBP1,GADD34,ATF-6).
主要成果:
- 在DENV感染期间,由于由病毒和错误折叠蛋白质引起的ER压力,UPR显著上调.
- 关键的UPR通路 (IRE1,PERK,ATF6) 被不受控制地激活,促进了自.
- DENV调节这些信号级联,导致失调的自.
结论:
- 经ER压力介导的UPR通路在登革热感染严重程度方面发挥着重要作用.
- 针对UPR途径和相关因素,为DENV.提供了一个潜在的治疗策略.
- 了解DENV的UPR调制对于开发新型抗病毒疗法至关重要.
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