Table 2 miRNA as a cholesterol regulation method in viral hepatitis

HBV

miR-205

Clinical HCC tissues showed an inverse correlation between ACSL4 and miR-205 expression levels. MiR-205 inhibited HBx’s ability to raise cellular cholesterol, a byproduct of ACSL4, in hepatoma cells. On the other hand, anti-miR-205 may elevate cellular cholesterol levels.

[85]

HBV and HCV

miR-27

The gene encoding the rate-limiting enzyme in cholesterol production, HMGCR, is controlled by miR-27, which is considerably downregulated in CHC, CHB, and HCC.

[78]

HCV

miR-185-5p

SREBP2 mRNA and protein expression were suppressed when miR-185-5p was overexpressed. SREBP2 protein expression was increased by miR-185-5p suppression. HCV core protein mediated the effects of miR-185-5p on SREBP2 expression.

[79]

HCV

miR-146a

Expression of miR-146a and intracellular cholesterol in PBMCs, as well as IFN concentration in sera, differ between genotype 1, HCV-infected patients, and healthy donors.

[80]

HCV

miR-122

In comparison to the pretreatment condition, the level of miR-122 expression in the PBMCs dropped following the antiviral therapy. In addition, six months after therapy, the amount of cholesterol in the PBMCs of CHC patients was greater than it was prior to treatment. Therefore, it would appear that one of the antiviral effects of the pegIFN-alpha/ribavirin therapies is the reduction of miR-122 expression in the PBMCs of CHC patients.

[83]