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J Virol. 2013 Jul;87(13):7338-47. doi: 10.1128/JVI.00378-13. Epub 2013 Apr 24.

Modulation of GB virus B RNA abundance by microRNA-122: dependence on and escape from microRNA-122 restriction.

Author information

1
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA. smsagan@stanford.edu

Abstract

Hepatitis C virus (HCV) RNA forms an unusual interaction with human microRNA-122 (miR-122) that promotes viral RNA accumulation in cultured human liver cells and in the livers of infected chimpanzees. GB virus B (GBV-B) is a hepatotropic virus and close relative of HCV. Thus, GBV-B has been used as a surrogate system to study HCV amplification in cultured cells and in infected tamarins. It was discovered that the 5'-terminal sequences of GBV-B RNA, like HCV RNA, forms an Argonaute 2-mediated complex with two miR-122 molecules that are essential for accumulation of GBV-B subgenomic replicon RNA. However, sequences in miR-122 that anneal to each viral RNA genome were different, suggesting distinct overall structural features in HCV:miR-122 and GBV-B:miR-122 complexes. Surprisingly, a deletion that removed both miR-122 binding sites from the subgenomic GBV-B RNAs rendered viral RNA amplification independent from miR-122 and Argonaute 2. This finding suggests that structural features at the end of the viral genome dictate whether miR-122 is required to aid in maintaining viral RNA abundance.

PMID:
23616647
PMCID:
PMC3700295
DOI:
10.1128/JVI.00378-13
[Indexed for MEDLINE]
Free PMC Article

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