Both seroprotection rate and GMT were higher in men as compared to women but the differences were not statistically significant (Table 1). == Table 1. antibody with geometric mean titer (GMT) of 55.44 77.01 mIU/mL. After booster vaccination, 97.1% of vaccinees developed protective levels of antibody and the GMT rose from 2.35 6.49 mIU/mL to 176.28 161.78 mIU/mL. 125/138 (90.6%) of re-vaccinated subjects also showed an anamnestic response to booster vaccination. At 20 years after primary vaccination with HB vaccine, low proportion of Brincidofovir (CMX001) the subjects had protective levels of antibody. However, the majority of the re-vaccinated subjects developed protective levels of anti-HBs and showed an anamnestic response after booster vaccination. Additional follow-up studies are necessary to determine the duration of immunological memory. Keywords:anamnestic response, anti-HBs antibody, hepatitis B vaccine, persistence, protection == Abbreviations == antibody to HBsAg antibody to HBcAg Hepatitis B Hepatitis B surface antigen Hepatitis B core antigen Hepatitis B virus Enzyme-linked immunosorbent assay Expanded Program on Immunization Geometric mean titer milli-international units per milliliter World Health Organization == Introduction == Hepatitis B virus (HBV) infection and its complications such as cirrhosis Brincidofovir (CMX001) and hepatocellular carcinoma has remained a major public health problem throughout the world. Approximately, one third of the world population shows a previous history of infection and more than 350 million individuals have been estimated to be chronically infected.1In areas with high endemicity, especially in some parts of Africa and south-east Asia, over 8% of individuals are chronically infected and the infection is predominantly transmitted vertically during prenatal period from carrier mothers to their neonates. In regions of intermediate endemicity, the patterns of the disease transmission is mixed and disease occurs at all ages, but again the predominant period of transmission seems to be at younger ages.2 Effective control of HBV transmission in regions with high and intermediate endemicity, therefore, would not be possible without vaccination of the vulnerable groups of the population.3The WHO (World Health Organization) strategy for effective control of HBV infection and its complications is the mass vaccination of neonates and children within the framework of Expanded Program on Immunization (EPI). In 1991, the Global Advisory Group to the WHO recommended that all countries integrate hepatitis B vaccine into national immunization by 1997.4,5This program has been incorporated in the national immunization scheme in Iran since 1993.6As of 2008, 177 countries worldwide have implemented HB immunization into their national immunization program as a routine vaccine given to all infants that lead to substantial reduction in the global burden and transmission of HBV.7 HBV expresses 3 forms of overlapping envelope proteins including the small (S antigen), middle (pre-S2 antigen) and large (pre-S1 antigen) proteins. The ‘S’ antigen (HBsAg) is the predominant form of the surface antigens and constitutes the immunodominant ‘a’ determinant required for induction of Brincidofovir (CMX001) protective antibody response in human.8,9The antibody response to HBsAg (anti-HBs) provides the immunity against HBV infection that appears after clearance of HBsAg or after immunization.8 Despite some differences in national vaccination programs between different countries, a 3 dose vaccination schedule (of 10 g or 20 g doses) of recombinant HBsAg are administered in most countries for vaccination of neonates and adults, respectively.6,8,10Vaccination with HBsAg induces protective antibody response (anti-HBs 10 mIU/mL) in the majority of vaccinees. The results obtained from several studies have indicated that vaccination of healthy neonates COL4A1 and adults with recombinant HBsAg induces a protective antibody response in 90-99% of vaccines.6,8,10We have previously reported a strong protective antibody response in the majority of healthy vaccinated neonates from Kerman and Urmia cities located in southeast and northwest of Iran, respectively.11However, a small proportion of vaccinees fail to respond, accounting for 1.7% and 3.9% of Urmian and Kermanian neonates, respectively.11We have also demonstrated that intramuscularly administration of a single supplementary low dose of HB vaccine induced high seroprotection rate in the non-responder neonates to primary course of vaccination.12 Although, vaccination with the HBsAg induces protection in the majority of vaccines, however, it has been shown that the anti-HBs level diminishes after vaccination. The results of the studies reported from different regions with varied hepatitis B endemicity have demonstrated the persistence of protection for at least 1015 years after primary vaccination despite diminishing antibody levels.13-16Some investigators have also suggested the need for a booster vaccination at 15 years after the completion of primary vaccination.17,18However, the determination of the protection duration after primary vaccination against HBV is important to evaluate whether booster vaccination may be necessary to extend protection through.