Chronic hepatitis B virus infection is an important global public health problem. Currently, after more than a decade of vaccination in China, the rate of hepatitis B surface antigen (HBsAg) positivity has decreased from 9.75% in the past to 7.18% now, and the total number of people has decreased from 120 million to more than 90 million. Although great progress has been made, due to the large population base in China, there are still about 30 million patients with chronic hepatitis B virus infection-related diseases, of which 10-20% will progress to cirrhosis, which is divided into compensated and decompensated stages, and the prognosis of these two stages is different, with a 5-year survival rate of 55% for compensated cirrhosis and 14% for decompensated cirrhosis. It has been confirmed that chronic infection with hepatitis B virus is the main cause of hepatitis B cirrhosis, and the 5-year incidence of decompensation is 4.05 times higher in HBV DNA-positive patients than in negative patients, and the mortality rate is 5.9 times higher, which shows that “HBV DNA load is a key factor affecting the progression of hepatitis B cirrhosis”. The need for aggressive antiviral therapy is even greater for patients with cirrhosis. Studies have shown that after 3 years of antiviral treatment in patients with compensated cirrhosis, if they are infected with a strain of virus without drug-resistant mutations, which is effective for treatment and has a low level of viral replication, only 5% of patients have disease progression, while 13% of patients with drug-resistant mutations have increased HBV DNA load, and 13% of patients have significant disease progression, including progression to decompensation or hepatocellular carcinoma, while The other 21% of patients without antiviral therapy showed disease progression. Therefore, we can conclude two things, one is that patients with cirrhosis should be actively treated with antiviral therapy, and the other is that continuous and effective inhibition of hepatitis B virus replication is the key. Ji Dong, Department of Hepatology, PLA 302 Hospital The antiviral therapy for patients with hepatitis B cirrhosis is different from that for patients without cirrhosis. The first requirement is that the viral replication level is high (>=105copies/ml for HBeAg positive patients and >=104copies/ml for HBeAg negative patients) and the second is that the transaminases should be elevated (ALT >=2ULN). In the case of patients with cirrhosis, we do not need to consider the level of transaminases, even if they are normal and even if the virus is not very high, we should start antiviral therapy. Next, from the point of view of the course of treatment, the general principle of both is the desire for long-term treatment. The only difference is that for patients with cirrhosis it is more important not to stop the medication easily. Once the medication is stopped, the recurrence, rebound or deterioration of the disease occurs, which can sometimes be fatal, because the liver reserve of cirrhotic patients’ function is significantly reduced and cannot withstand repeated blows, and it is more important to emphasize that the medication should not be stopped at will. Here again, two points are emphasized: one is that cirrhotic patients should consider antiviral therapy as long as they are virus positive; the other is that antiviral therapy for cirrhotic patients is a long-term treatment with no fixed course and should not be discontinued at will, even for life in the decompensated stage.