Interferon (IFN-α) and antiviral drugs (nucleoside (acid) analogs) are currently the basic means of treating chronic hepatitis B virus infection. Interferon therapy is currently the treatment method with the highest sustained response rate after drug treatment. After treatment, it can be accompanied by surface antigen turning negative, which is also the ultimate goal of current treatment of chronic hepatitis B. However, the effect of interferon on hepatitis B patients is very different, and its mechanism of action is not completely clear.
Based on the previous work (Hepatology, 55: 730-741), Meng Songdong ’s research group Hao Junli and others found that interferon significantly reduced the level of the most abundant and specifically expressed small RNA-miR-122 in liver cells, and further studies found that interference The hormone does not mainly regulate miR-122 at the transcription level, but by up-regulating the expression of at least one interferon-activated gene (ISG) -NT5C3. Interestingly, the 3'-UTR of NT5C3 mRNA contains the target of miR-122, and the abundantly expressed NT5C3 mRNA inhibits and down-regulates miR-122 in a "sponge" adsorption. Since miR-122 significantly inhibits the expression and replication of hepatitis B virus, the down-regulation of miR-122 has a great negative effect on the antiviral effect of interferon, which partly explains the reason for the large difference in the effect of interferon on hepatitis B. This study also provides a basis for enhancing the antiviral efficacy of interferon.
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