Chronic hepatitis B is a global health problem that can eventually progress to cirrhosis or hepatocellular carcinoma. HBV enters hepatocytes and forms intrahepatic covalent closed-loop DNA (CCC DNA) that is difficult to clear. In recent years, a growing number of studies have shown that the clinical relevance of HBsAg levels is reflected in its association with intrahepatic covalent closed-loop DNA (CCC DNA), which is the primary template for HBV replication. Through this correlation, HBsAg is considered a marker of immune response against HBV therapy. The level of HBsAg in the serum of patients with chronic HBV infection is highly correlated with intrahepatocellular DNA (cccDNA), and the disappearance of HBsAg reflects the clearance of cccDNA and viral infection of hepatocytes. In an interview with H International Liver Disease, academician Wen Yumei suggested that the treatment of chronic hepatitis B should be “two-handed” – one hand to reduce viral load, and the other hand to improve T-cell immunity. The serological conversion of HBsAg indicates that T-cell function is very strong and the immune control status is achieved, which often means a good prognosis. In recent years, hepatologists at home and abroad have made HBsAg conversion and serological conversion the highest goal in the treatment of chronic hepatitis B. It is well known that the only two types of anti-hepatitis B virus drugs available worldwide are interferons and nucleoside analogues. In terms of the mechanism of action, these are two completely different types of drugs, nucleoside analogs mainly through the competitive inhibition of NBV DNA polymerase, reduce the replication of HBV DNA to play an antiviral role, but can not remove the intracellular HBV cccDNA, and after discontinuation of the drug to start the cycle of viral replication; while interferon both inhibit the role of viral replication, blocking the process of virus reinfection, but also can induce immune response In contrast, interferon both inhibits viral replication, blocks the process of viral reinfection, and induces an immune response that effectively clears infected hepatocytes, resulting in higher HbsAg clearance rates. Last year, a foreign study showed that interferon can make cccDNA more “restricted” and the virus becomes inactive, producing very little transcript, so that HBsAg disappears. Therefore, our hospital uses antiviral treatment with nucleoside analogues for patients with chronic hepatitis B. The replication of HBVDNA is quickly suppressed and maintained for a long time, thus indirectly depleting cccDNA in liver cells as much as possible; at the same time, HBsAg levels are monitored and interferon is used sequentially at the right time to further clear HBsAg. The results of our 48-week treatment showed that this sequential treatment resulted in 33.3% seroconversion of HBsAg, which is much higher than that of interferon alone for one year (8-15%) or nucleoside analogs alone for HBsAg negative conversion (2-8%). The results we obtained are similar to those of the OSST study led by Ning Qin. For this group of cases we will adjust the treatment regimen according to the changes in HBsAg concentration.