Hepatitis B is a relatively complex disease that causes great suffering and burden to the lives of patients. Approximately 400 million people worldwide are afflicted by hepatitis B virus (HBV) infection, with almost all perinatal mother-to-child transmission infections and 50% of those infected between the ages of 1-5 years becoming chronic. Chronic HBV infection is a diverse and variable dynamic process that can progress from inactive carrier status to chronic hepatitis B, leading to cirrhosis and hepatocellular carcinoma; it can occur after HBeAg serologic conversion with anti-HBe antibodies, or after years or decades of inactive carrier status, with “HBeAg-negative chronic hepatitis B “HBVDNA can still be detected in the liver even during the “HBsAg-negative phase” after HBsAg disappears; if cirrhosis has occurred before HBsAg disappears, the patient is still at risk of developing liver cancer. Due to the persistence of covalent closed-loop DNA in the nucleus of infected hepatocytes, chronic HBV infection cannot be completely eradicated yet, which determines the necessity of long-term follow-up. Screening of high-risk groups All first-degree relatives and sexual partners of persons with chronic HBV infection, as well as those who have had pedicures, tattoos, pierced earrings, accidental exposure in the work of medical personnel, and shared razors and toothbrushes, should be tested for HBV serum markers (HBsAg, anti-HBc, anti-HBs). If these markers are negative, hepatitis B vaccination should be administered. Assessment of chronic HBV infected patients 1.Assessment of severity of liver disease: biochemical indicators including glutamic aminotransferase (AST) and ALT, gamma-glutamyl transpeptidase (GGT), alkaline phosphatase, bilirubin, and serum albumin and globulin, blood count and prothrombin time, and liver ultrasound (including assessment of the degree of fibrosis). 2.HBVDNA test. 3.Systematic examination for other causes of chronic liver disease, including co-infection with HDV, HCV and/or HIV, alcoholic, autoimmune, fatty liver or steatohepatitis and other metabolic liver diseases. 4. Liver biopsy if necessary to clarify the severity of inflammatory necrosis and fibrosis to determine whether to start treatment. Timing of treatment 1. Patients with positive HBeAg, high HBVDNA, persistently normal ALT (tested at least every 3 months and for at least 1 year), no evidence of liver disease and no family history of liver cancer or cirrhosis do not require immediate treatment. However, they must be followed up at least every 3-6 months. Liver biopsy or even treatment should be considered in these patients who are older than 30 years and/or have a family history of liver cancer or cirrhosis. 2. Patients who are HBeAg negative, have HBVDNA less than 20,000 IU/ml, have persistently normal ALT, no evidence of liver disease and no family history of liver cancer or cirrhosis do not need immediate liver biopsy or treatment. However, they must be followed closely, with ALT testing every 3 months and HBVDNA testing every 6-12 months for at least 3 years. After 3 years, as with all inactive chronic HBV carriers, lifelong follow-up is warranted. 3, HBeAg-positive and HBeAg-negative chronic hepatitis B patients with ALT greater than 2 times the upper limit of normal and serum HBVDNA greater than 20,000 IU/ml can start treatment. 4. Patients with compensated cirrhosis with detectable HBVDNA must be considered for antiviral therapy; patients with decompensated cirrhosis with detectable HBVDNA require urgent antiviral therapy with nucleoside (acid) analogues. Monitoring treatment effects and adverse drug reactions 1. Patients treated with pegylated interferon should have their complete blood count and serum ALT levels tested monthly, TSH every 3 months, HBeAg, anti-HBe, HBsAg and serum HBVDNA levels tested every 3-6 months, and treatment should be directed according to response (RGT strategy). At 24 weeks of pegylated interferon treatment for HBeAg-positive hepatitis, if HBsAg decreases to <1500 IU/ml, it has a high probability of achieving HBsAg conversion, and patients should be encouraged to continue treatment until 48 weeks. For those who experience HBeAg serological conversion at 48 weeks of treatment and HBsAg quantification continues to decrease significantly to below 250 IU/ml, treatment can be extended to 72 weeks or If HBsAg decreases to 1500-20,000 IU/ml, patients can be encouraged to extend the treatment time; if HBsAg >20,000 IU/ml, the possibility of treatment response is very small, and treatment should be replaced by or combined with nucleoside (acid) analogues. When pegylated interferon is used to treat HBeAg-negative hepatitis, if the quantitative decrease of HBsAg >1log10IU/mL at 24 weeks of treatment, continue treatment until 48 weeks. For those patients whose HBsAg quantification is still >10IU/mL at 48 weeks of treatment, but HBsAg quantification still continues to decrease steadily, treatment can be extended to 72 weeks. If the HBsAg quantification decreases ≤1log10IU/mLl at 24 weeks of treatment, the treatment should be switched to or combined with nucleoside (acid) analogues. If HBsAg quantification is <10IU/ml at 48 weeks of treatment, 80% can show a durable virological response; on the contrary, no one shows a durable virological response in patients whose HBsAg is still >5000IU/ml at 48 weeks of treatment. 2, nucleoside (acid) analog therapy patients, in addition to routine monitoring of liver function, renal function, AFP, liver ultrasound and other items, should be tested every 6 months for HBsAg, HBeAg and anti-HBe, every 3-6 months for HBVDNA, should also be monitored at the same time muscle enzymes and blood phosphorus. The key to dealing with the problem of drug resistance of nucleoside (acid) analogues is, in addition to choosing a strong drug with low resistance rate according to the disease, the most important thing is to review it regularly, and the HBVDNA can be reduced to less than 10C15IU/ml to avoid drug resistance. If poor response or “virological breakthrough” is detected during monitoring, early adjustment is required. Nucleoside (acid) analogs are metabolized by the kidneys and all patients should be evaluated for renal risk at baseline and monitored at 3-month intervals during the first year of treatment and every 6 months thereafter in the absence of deterioration.