[9] A number of other miR-122 targets, including CD320, AldoA and BCKDK, have been identified by microarray analysis of changes in mRNA expression in the liver of mice treated with miR-122 inhibitors.

[10][11][12] The overall effect of miR-122 inhibition is to reduce the plasma cholesterol level, although the pathways involved in this regulation have not been fully elucidated.

[17][18][19] Recent studies demonstrated that miR-122 may directly regulate different aspects of the interferons (IFNs) signaling pathway[20][21] to enhanced induction of anti-viral genes and inhibition of various virus.

[21][22][23][24][25][26][27][28][29][30] Moreover, miR-122 have been shown to target various genes,[31][32][29][33][28] resulting in enhancement of IFN signaling and subsequent antiviral innate immunity.

[45] The crystal structure of Ago2:miR-122 bound to the miR-122 binding site at the 5'-end of the HCV genome, in combination with functional experiments, suggests that the viral RNA has evolved to maximize protection from cytoplasmic exoribonucleases by altering the molecular behavior of Ago2.

[47] The existing HCV therapy of PEG-IFNα plus ribavirin is poorly tolerated and frequently ineffective,[48][26] so there is an urgent need for new drugs, and miR-122 inhibitors are an attractive possibility.

The association between low miR-122 levels and hepatocellular carcinoma suggests that caution will be necessary when testing miR-122 inhibitors, and that long-term treatment might be undesirable.

However, miR-122 is a promising target as it can be very selectively and effectively inhibited with antisense oligonucleotides, and as it is a conserved host factor it is hoped that the virus would not be able to acquire resistance mutations to an anti-miR-122 therapeutic.

[22][23][24][31][27] As of 2017, Santaris Pharma was developing miravirsen, a locked nucleic acid-based antisense oligonucleotide that inhibits miR-122, as a potential treatment for HepC.

[57] In addition, decreased levels of miR-122 in liver biopsies have been linked to a strain of hepatitis C that is resistant to interferon therapy.

The commonly used anticoagulant heparin profoundly inhibits the by reverse transcription polymerase chain reaction (RT-PCR) used for microRNA quantification.