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实验性登革热病毒4型感染增加了微RNAs-15/16的表达,触发了酶诱导的亡途径

Samir Mansour Moraes Casseb^1,2, Karla Fabiane Lopes de Melo¹, Carlos Alberto Marques de Carvalho³

¹Experimental Pathology Section, Evandro Chagas Institute, Ananindeua 67030-000, PA, Brazil.

Current issues in molecular biology

|June 27, 2023

概括

肝细胞中的登革热病毒 (DENV) 感染导致微RNAs-15/16的过度表达. 这些miRNA与病毒载量,NS1蛋白水平和亡相关,表明它们作为登革热损伤标记物的潜力.

科学领域:

病毒学病毒学
分子生物学分子生物学
肝病学肝病学是一种肝病学.

背景情况:

登革热病毒 (DENV) 在全球造成数百万例感染,构成了严重的公共卫生威胁.
DENV有四种血清型,由蚊子传播,使其成为蚊子传播的最普遍的疾病.
DENV非结构蛋白1 (NS1) 与严重的登革热症状有关.

研究的目的:

为了研究4型登革热病毒 (DENV-4) 感染,NS1蛋白,microRNAs-15/16 (miRNAs-15/16) 和人类肝细胞中亡之间的关系.
为了确定miRNAs-15/16是否可以作为肝细胞中DENV感染的生物标志物.

主要方法:

人类肝细胞系 (Huh 7.5 和 HepG2) 感染了 DENV-4.
在感染后的时间内量化miRNAs-15/16,病毒载量,NS1蛋白和caspases-3/7活动.

主要成果:

DENV-4感染导致miRNAs-15/16在HepG2和Huh 7.5细胞中的过度表达.
miRNAs-15/16水平与NS1蛋白表达和病毒载量存在相关性.
微RNAs-15/16的表达也与caspases-3/7的活性有关,这表明它在亡中发挥了作用.

结论:

在人类肝细胞中,miRNAs-15/16在DENV-4感染期间显著上调.
这些微RNA与病毒复制和细胞损伤的关键指标有关.
miRNAs-15/16代表了评估登革热病毒感染中肝损伤的潜在生物标志物.

关键词:

灭症 (apoptosis) 是一种死亡的过程.登革热病毒 (DENV) 病毒微RNAs 是一个微型RNA.病毒的非结构性蛋白质.

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