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miR-122 stimulates hepatitis C virus RNA synthesis by altering the balance of viral RNAs engaged in replication versus translation.

Abstract：

:The liver-specific microRNA, miR-122, stabilizes hepatitis C virus (HCV) RNA genomes by recruiting host argonaute 2 (AGO2) to the 5' end and preventing decay mediated by exonuclease Xrn1. However, HCV replication requires miR-122 in Xrn1-depleted cells, indicating additional functions. We show that miR-122 enhances HCV RNA levels by altering the fraction of HCV genomes available for RNA synthesis. Exogenous miR-122 increases viral RNA and protein levels in Xrn1-depleted cells, with enhanced RNA synthesis occurring before heightened protein synthesis. Inhibiting protein translation with puromycin blocks miR-122-mediated increases in RNA synthesis, but independently enhances RNA synthesis by releasing ribosomes from viral genomes. Additionally, miR-122 reduces the fraction of viral genomes engaged in protein translation. Depleting AGO2 or PCBP2, which binds HCV RNA in competition with miR-122 and promotes translation, eliminates miR-122 stimulation of RNA synthesis. Thus, by displacing PCBP2, miR-122 reduces HCV genomes engaged in translation while increasing the fraction available for RNA synthesis.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Masaki T,Arend KC,Li Y,Yamane D,McGivern DR,Kato T,Wakita T,Moorman NJ,Lemon SM

doi

10.1016/j.chom.2014.12.014

subject

Has Abstract

pub_date

2015-02-11 00:00:00

pages

217-28

issue

2

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(15)00020-7

journal_volume

17

pub_type

杂志文章

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