Modulation of Hepatitis C Virus RNA Abundance and the Isoprenoid Biosynthesis Pathway by MicroRNA miR-122 Involves Distinct Mechanisms
Modulation of Hepatitis C Virus RNA Abundance and the Isoprenoid Biosynthesis Pathway by MicroRNA miR-122 Involves Distinct Mechanisms
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DOI：
10.1128/jvi.01156-09
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发表时间：
2010-01-01
影响因子：
5.4
通讯作者：
Sarnow, Peter
中科院分区：
文献类型：
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作者：
Norman, Kara L.;Sarnow, Peter
MicroRNA 122 （miR-122）通过与病毒RNA的直接相互作用促进丙型肝炎病毒（HCV） RNA丰度，并刺激动物肝脏中的甲羟戊酸途径。我们发现，miR-122的过表达增强了病毒RNA的积累，而不影响甲羟酸途径中的基因，如3-羟基-3-甲基戊二酰辅酶A还原酶（HMGCR）基因。然而，抑制miR-122可以降低HCV RNA和HMGCR RNA，但对HCV和HMGCR RNA的合成率影响不大。类异戊二烯中间代谢物不能恢复HCV RNA的丢失。总的来说，这些发现表明miR-122调节病毒RNA丰度独立于其对类异戊二烯代谢的影响。
MicroRNA 122 (miR-122) promotes hepatitis C virus (HCV) RNA abundance through a direct interaction with the viral RNA and stimulates the mevalonate pathway in the animal liver. We found that overexpression of miR-122 enhanced viral RNA accumulation without affecting genes in the mevalonate pathway, such as the 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) gene. However, inhibition of miR-122 decreased both HCV RNA and HMGCR RNA with little effects on the rates of HCV and HMGCR RNA synthesis. Loss of HCV RNA could not be restored by isoprenoid intermediate metabolites. Overall, these findings suggest that miR-122 modulates viral RNA abundance independently of its effect on isoprenoid metabolism.