What are the main objectives of antiviral therapy in patients with chronic hepatitis B cirrhosis? HBV infection is an important cause of cirrhosis. The 5-year incidence of chronic HBV infection progressing to cirrhosis ranges from 8% to 38%. Persistently high viral load is a major risk factor for the development of cirrhosis and is independently predictive of cirrhosis. Additional risk factors that predispose chronic HBV-infected individuals to progression to cirrhosis include: immune status (repeated or sustained immune clearance), male gender, age >40 years, alcoholism, and comorbid hepatitis C, with genotype C being at greater risk. Loss-of-compensation cirrhosis is usually the result of insidious progression of compensated cirrhosis, and a number of predisposing factors can lead to progression, with 2% to 5% of patients with compensated cirrhosis progressing to loss-of-compensation each year; 20% of patients with compensated cirrhosis progress to loss-of-compensation within 5 years of diagnosis, and as many as 60% after 10 years.The median survival of patients with HBV-associated cirrhosis is 10 to 12 years. Once progression to decompensation occurs, patients often develop complications due to portal hypertension and have a significantly increased risk of death. The 5-year survival rates for patients with compensated and decompensated cirrhosis are 84% and 14%, respectively. Therefore, according to Prof. Lok, “Detecting active mild compensated cirrhosis and preventing its progression may be the last step in effectively saving the natural life cycle. High risk factors for the development of decompensated cirrhosis include advanced age, male gender, HBeAg(+), alcohol abuse and ineffective antiviral therapy.” Effective suppression of HBV replication improves hepatic fibrosis.NA long-term treatment stabilizes or reduces the degree of esophageal varices in most patients with compensated cirrhosis.NA long-term treatment reverses most stage F1-F3 liver fibrosis, and stage F4 liver fibrosis can be reversed with variable efficacy, and a small proportion of patients with cirrhosis may have a reduction in portal hypertension, whereas severe portal hypertension is irreversible . The problem with cirrhotic patients is that they are all in the end-stage liver disease stage because the virus continues to replicate actively for many years. This suggests that hepatocytes contain a large number of viruses and, due to the unique biology of HBV, many viral sequences can be integrated into the host’s genome, greatly increasing the risk of hepatocellular carcinoma (HCC). Also, cirrhosis is a risk factor for HCC due to the formation of intrahepatic arteriovenous short circuits and structural changes. In addition, HBV virus also has a direct to cancerous effect. Therefore, the main goal of safe and effective antiviral therapy is to reduce the viral activity and the incidence of decompensated liver disease in these patients, as well as to reduce the risk of HCC. In addition to aggressive antiviral therapy, it is strongly recommended that cirrhotic patients should be screened every 6 months. HCC is an important clinical outcome in HBV-associated cirrhosis, and both compensated and decompensated cirrhosis are at risk of progressing to HCC. A Taiwanese study showed that baseline HBVDNA >10,000 copies/ml was the strongest independent predictor of HCC occurrence after adjusting for age, gender, smoking, alcohol consumption, HBeAg status and serum ALT level. Very high risk groups for hepatocarcinogenesis include: cirrhosis with a family history of hepatocellular carcinoma or males >50 years of age; hepatitis B cirrhosis with positive DNA; cirrhotic nodules less than 1 CM detectable on imaging; cirrhotic decompensated events, or comorbid diabetes mellitus. In particular, patients with hepatitis B cirrhosis who are DNA-negative after antiviral therapy also belong to the high-risk group.