Tuesday, March 17, 2015

Hep C RNA "sequesters" miR-122

As we learned in class, Hepatitis C virus (HCV) conducts microRNA-122 (miRNA-122)-dependent replication in the liver. More specifically, the HCV viral particle must actually physically bind to miRNA-122 in order to initiate replication. A heretofore unrealized consequence of this attraction is the "sequestration" of miRNA-122, or the "pulling away" of this molecule from its normal day job, which is to regulate genes. The consequences of this effect may be far-reaching and may underlie HCV pathology.

An article in the March 2015 issue of Cell, "Hepatitis C Virus RNA Functionally Sequesters miR-122," by Luna et al. establishes this phenomenon. The researchers, who conducted their work at Rockefeller University, posit that their conclusions suggest strongly that miRNA-122 should be a target molecule in drug development.

microRNA is an RNA subtype specifically equipped to dampen gene expression by recruiting "silencing proteins" to an mRNA transcript before it can be translated. miRNA-122 in particular governs the gene expression of factors involved in crucial functions like iron and cholesterol metabolism and circadian rhythms.
This image is the "graphical abstract" submitted by the Luna group and aptly summarizes the main take-away from this article.

--Shubha Raghvendra

Source: Luna, J M et al. "Hepatitis C Virus RNA Functionally Sequesters miR-122." Cell. 2015: vol. 160, no. 6. http://www.sciencedirect.com/science/article/pii/S0092867415001919.

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