Observation on the role of miR-16-5p in the replication of Zika virus / 中国输血杂志

ABSTRACT

【Objective】 To investigate the role of non-coding microRNA miR-16-5p in ZIKV replication and the underlying mechanism. 【Methods】 1×105/mL HeLa cells were seeded in 24-well plate and infected with ZIKV(MOI=5). RNAs were harvested, and miR-16-5p expression levels were measured by qRT-PCR at 24, 48 and 72 hour post infection, respectively. HeLa cells were transfected with 20nM miR-16-5p mimic and infected with ZIKV(MOI=5) at 24h post transfection. RNAs were extracted and ZIKV RNA and several inflammation factors expression were tested using qRT-PCR at 48h post infection. HeLa cells were co-transfected with 1μg NFκB-luc and 10ng pRL-TK with 20nM miR-16-5p mimic, and then infected with ZIKV(MOI=5) for 24h before the luciferase expression was tested at 48h post infection. HeLa cells were transfected with 20nM miR-16-5p mimic and infected with ZIKV(MOI=5) at 24h post transfection, and cell apoptosis was assayed through flow cytometry. 【Results】 Compared with uninfected control, miR-16-5p expression was significantly decreased at 24h, 48h and 72h following ZIKV infection. MiR-16-5p over-expression inhibited ZIKV replication, while upregulated NFκB activity and inflammation factors expression compared with the negative mimic-transfected cells. MiR-16-5p overexpression also promoted HeLa cell apoptosis. 【Conclusion】 ZIKV infection downregulated intracellular miR-16-5p expression. Overexpression of miR-16-5p suppressed ZIKV infection. MiR-16-5p inhibited ZIKV replication and promoted cell apoptosis probably by activating NFκB pathway and stimulating inflammation factors expression.