Published online Jul 26, 2021. doi: 10.12998/wjcc.v9.i21.5812
Peer-review started: February 24, 2021
First decision: April 18, 2021
Revised: May 2, 2021
Accepted: May 26, 2021
Article in press: May 26, 2021
Published online: July 26, 2021
Recent studies analyzed serum soluble programmed death-1 (sPD-1) levels and indicated that sPD-1 might play an important role in virus-specific immunity in chronic viral infection.
The factors that contribute to the functional cure in patients with chronic hepatitis B remain unclear, and the predictors of functional cure are worth exploring.
To investigate the factors associated with hepatitis B surface antigen (HBsAg) loss and explore the impact of sPD-1 Levels.
Patients with positive hepatitis B e antigen (HBeAg) levels at baseline and with available sequential samples who achieved HBsAg loss during antiviral treatment served as the case group. This case group (n = 11) was further matched to 44 positive HBeAg patients without HBsAg loss as controls.
Patients with HBsAg loss had higher levels of sPD-1 than patients without HBsAg loss from baseline to month 96, and the differences were significant between the groups at baseline (P = 0.0136), months 6 (P = 0.0003), 12 (P < 0.0001), 24 (P = 0.0007), 48 (P < 0.0001), and 96 (P = 0.0142). The sPD-1 levels were positively correlated with ALT and HBV DNA levels in patients with HBsAg loss within 12 mo of antiviral treatment. After 12 mo of antiviral treatment, the sPD-1 levels were negatively correlated with HBsAg levels in all patients, especially at 24 (r = -0.356, P = 0.0497) and 48 (r = -0.4783, P = 0.0037) mo. The AUC of sPD-1 levels at 6 mo for HBsAg loss was 0.898 (P = 0.000), whereas that of HBsAg was 0.617 (P = 0.419). The cut-off value of sPD-1 was set at 2.34 log pg/mL; the sensitivity and specificity were 100% and 66.7%, respectively.
The sPD-1 levels were significantly different between the two groups of patients during antiviral treatment, especially within 12 mo after baseline. The sPD-1 levels at 6 mo can predict HBsAg loss after 144 mo of antiviral treatment.
The correlation between sPD-1 levels and HBsAg loss depended on the immune response of functional HBV-specific T cells to HBV infection. The T cell function of patients from this study needed to be detected.