The hepatitis B virus has been integrated with the nucleus of human liver cells. After the death of aging liver cells, new liver cells are generated and the hepatitis B virus is regenerated together with liver cells, so the hepatitis B virus exists in liver cells for a long time or even for life. HBVDNA is a sign of hepatitis B virus replication. There are different degrees of replication, fast and slow, high and low. HBVDNA is a condition for antiviral treatment, but it is not a decisive condition. Antiviral therapy can only be administered if HBVDNA reaches a certain level of titers while ALT is elevated to twice the upper limit of normal or higher or if liver puncture has G2, S2 or moderate liver elastic fibrosis (liver stiffness); patients with evidence of cirrhosis can be treated with antiviral therapy without regard to HBV DNA and ALT. HBVDNA can also be used as one of the criteria for judging the efficacy of antiviral therapy. A gradual decrease in HBVDNA indicates that antiviral therapy is effective; if HBVDNA does not drop all the time after many months of antiviral therapy, it indicates poor efficacy; if HBVDNA drops faster in a short period of time, it indicates better antiviral efficacy; but if HBVDNA drops and then rebounds to rise by a factor of 10, it indicates the occurrence of drug resistance. In short, whether antiviral treatment does not depend on HBV DNA, does not meet the conditions of treatment, can not be blindly treated, must wait for the right time, otherwise treatment can only be the opposite, reduce the efficacy of treatment, drug resistance, disrupt the body’s own immune balance, and even lifelong incurable.