Clinical utility of hepatitis B surface antigen kinetics in treatment-naïve chronic hepatitis B patients during long-term entecavir therapy

Figure 1 Cumulative incidence of virological response. A: Cumulative incidence of virological response in HBeAg-positive patients; B: Cumulative incidence of virological response in HBeAg-positive non-cirrhotic patients; C: Cumulative incidence of virological response in HBeAg-negative patients; D: Cumulative incidence of virological response in HBeAg-negative non-cirrhotic patients.

Figure 2 Cumulative incidence of HBeAg serological response. A: Cumulative incidence of HBeAg seroclearance; B: Cumulative incidence of HBeAg seroconversion.

Figure 3 HBsAg kinetics during entecavir treatment. A: HBsAg levels at different time points, categorized by baseline HBeAg and cirrhosis status; B: Annual HBsAg changes in different periods, categorized by baseline HBeAg and cirrhosis status; C: HBsAg levels and annual HBsAg changes, categorized by baseline HBsAg < 3 log IU/mL and ≥ 3 log IU/mL; D: HBsAg levels and annual HBsAg changes, categorized by time to virological response < 6 mo and ≥ 6 mo; E: HBsAg levels and annual HBsAg changes, categorized by HBeAg seroconversion in HBeAg-positive non-cirrhotic patients. Error bars represent 95% confidence intervals. Comparisons between different time points or periods for one patient group: ^aP < 0.05, ^bP < 0.005, ^cP < 0.001; Comparisons between different groups at one specific time point or period: ^dP < 0.05, ^eP < 0.005, ^fP < 0.001.

Figure 4 Possible mechanisms for HBsAg decline after nucleos(t)ide analogue treatment. A: Nucleos(t)ide analogues inhibit the activity of HBV reverse transcriptase; B: The production of relaxed circular DNA; C and D: The package andrelease of complete virions, and the replenishment of cccDNA. cccDNA: Covalently closed circular DNA; HBc: Hepatitis B core protein; HBsAg: Hepatitis B surface antigen; L/M/S proteins: Large, middle, and small envelope proteins; HBV: Hepatitis B virus.