The Coexistence of Hepatitis B Surface Antigen and Anti-HBs in Patients With Chronic HBV Infection: Prevalence and Related Factors

Background and AimsThe prevalence of coexistence of HBsAg and anti-HBs in chronic hepatitis B virus (HBV)–infected patients is different between studies. The mutations on the S gene were proved as the cause of this coexistence. This study determined the frequency and factors associated with coexistence of HBsAg and anti-HBs in chronic HBV-infected patients.MethodsThis cross-sectional study was conducted at University Medical Center at Ho Chi Minh City, Vietnam, from April 2014 to December 2020. HBeAg, HBsAg, and anti-HBs were measured by chemiluminescent immunoassay. Mutations on the HBV small S gene from amino acids 1–227 were detected using Sanger sequencing on 177 patients.ResultsA total of 521 chronic HBV-infected patients were enrolled, including 350 males (62.7%), 17.1% with hepatic fibrosis of ≥ F3 and 9.8% with hepatocellular carcinoma (HCC). The coexistence of HBsAg and anti-HBs was detected in 9.8%, with 17.9% among genotype C compared to 7.4% in genotype B, P = .001. The coexistence group had lower levels of HBsAg titers (P = .052). There were significantly higher rates of coexistence in the group with HCC (19.6% vs 8.7%, P = .013). The existence of point mutations on the major hydrophilic region and the “a” determinant region of HBV was more frequently detected in the HBsAg and anti-HBs coexistence group (P = .043 and P = .008, respectively).ConclusionThe coexistence of HBsAg and anti-HBs was detected more frequently in the HBV genotype C group. The coexistence status was related to lower HBsAg titers, mutations on the major hydrophilic region, and/or the “a” determinant and exposed significant relation with HCC. The prevalence of coexistence of HBsAg and anti-HBs in chronic hepatitis B virus (HBV)–infected patients is different between studies. The mutations on the S gene were proved as the cause of this coexistence. This study determined the frequency and factors associated with coexistence of HBsAg and anti-HBs in chronic HBV-infected patients. This cross-sectional study was conducted at University Medical Center at Ho Chi Minh City, Vietnam, from April 2014 to December 2020. HBeAg, HBsAg, and anti-HBs were measured by chemiluminescent immunoassay. Mutations on the HBV small S gene from amino acids 1–227 were detected using Sanger sequencing on 177 patients. A total of 521 chronic HBV-infected patients were enrolled, including 350 males (62.7%), 17.1% with hepatic fibrosis of ≥ F3 and 9.8% with hepatocellular carcinoma (HCC). The coexistence of HBsAg and anti-HBs was detected in 9.8%, with 17.9% among genotype C compared to 7.4% in genotype B, P = .001. The coexistence group had lower levels of HBsAg titers (P = .052). There were significantly higher rates of coexistence in the group with HCC (19.6% vs 8.7%, P = .013). The existence of point mutations on the major hydrophilic region and the “a” determinant region of HBV was more frequently detected in the HBsAg and anti-HBs coexistence group (P = .043 and P = .008, respectively). The coexistence of HBsAg and anti-HBs was detected more frequently in the HBV genotype C group. The coexistence status was related to lower HBsAg titers, mutations on the major hydrophilic region, and/or the “a” determinant and exposed significant relation with HCC.