The discovery and use of interferon was a milestone in antiviral therapy, “To date, no other scientific discovery has had such a significant impact on the treatment of viral hepatitis as interferon” (quoted from the 2007 American Liver Congress brochure). Interferon has a wide range of actions, with its antiviral, antiproliferative, antitumor, and immunomodulatory activities. The main mechanism of interferon against HBV: Interferon activates Jakl and Tyk2 by binding to class I interferon receptors on the cell membrane, and these two signaling molecules activate signal transduction and transcriptional activators STAT1 and STAT2 in the cytoplasm, and the latter two enter the nucleus of the cell and bind to interferon susceptibility response elements (IFNSREs) in the human genome to induce a series of antiviral proteins, such as mucin, tocopherol, tocopherol, tocopherol, tocopherol, tocopherol, tocopherol, tocopherol, tocopherol, tocopherol and tocopherol. A series of antiviral proteins, such as the mucovirus resistance gene (MxA) product, 2 5 oligoadenylate synthetase (2 5 OAS), and RNA-dependent protein kinase (PKR), inhibit transcription of the HBV gene, degrade HBV mRNA, and inhibit translation of HBV proteins, respectivelyI . Meanwhile, interferon has immunomodulatory functions, including up-regulation of HLA-class I and II antigen expression, promotion of NK cells and NK T lymphocytes, cytotoxic T lymphocytes, and macrophage activity. Application of IFN in the treatment of chronic hepatitis B: At present, interferons approved for the treatment of chronic hepatitis B in China include ordinary IFN and PEG-IFN. For HBeAg-positive chronic hepatitis B, the meta-analysis found that the sustained response rate of IFN (the sustained negative rate of HBeAg and HBV DNA at 24 weeks after the cessation of treatment) in patients with persistent or intermittent elevation of ALT was 37%, which was significantly higher than that of 17% in the placebo group. For HBeAg-negative chronic hepatitis B, four randomized controlled trials showed that HBV DNA conversion rates at the end of IFN treatment ranged from 38% to 90%, compared with 0-37% in the control group; however, nearly half of the responders relapsed at the end of treatment. Extending the course of treatment to 12 to 24 months may increase the rate of sustained response in patients with HBeAg-negative chronic hepatitis B. IFN for chronic hepatitis B has a favorable long-term outcome. It has been reported that after 4 to 8 years of follow-up, 80% to 90% of patients remain HBeAg-negative, but HBV DNA can still be detected in serum by PCR in the majority of these patients. studies in Europe and the United States have shown that up to 12% to 65% of patients can become HBsAg-negative within 5 years of HBeAg conversion. A study in Taiwan followed 233 cases of interferon-treated HBeAg-positive chronic hepatitis B for 1.1 to 16.8 years (median 6.8 years) and found that the incidence of cirrhosis and hepatocellular carcinoma was significantly lower in those who had achieved seroconversion of HBeAg, and that seroconversion of HBsAg had occurred in l0% of the patients. However, some authors have reported that no long-term clinical benefit of IFN was observed in Asian patients. The recommended treatment regimen in China is IFN 5 MU every other day, subcutaneously or intramuscularly, for 24 weeks (HBeAg-positive patients) or a total of 48 weeks (HBeAg-negative patients). PEG-IFN for HBeAg-positive chronic hepatitis B: In a phase III clinical trial, treatment of HBeAg-positive chronic hepatitis B (87% Asian) with PEG-IFN I2a (40 × 10 ) for 48 weeks and discontinuation of the drug for 24 weeks of follow-up resulted in an HBeAg serologic conversion rate of 32%; for In 172 of these cases, 82.4% (56/68) of the patients who had achieved HBeAg seroconversion at 12 months post-discontinuation remained HBeAg-converted, and 14% (14/103) of the patients who had not achieved HBeAg seroconversion had achieved HBeAg seroconversion. Thus, a total of 42% (73/172) had achieved HBeAg seroconversion at 12 months after discontinuation of the drug.1 Similar short-term efficacy of PEG-IFN1b in chronic hepatitis B has been reported in the literature. In HBeAg-negative chronic hepatitis B, in a phase III clinical study, HBeAg-negative patients (60% Asian) were treated with PEG-IFN1b (40 × 103) for 48 weeks and then followed up for 24 weeks, and HBV DNA was not significantly reduced.