To investigate the efficacy in anti-HBsAg response with half the recommended adult dose in a standard vaccination schedule or with a full dose in reduced number of vaccination schedule, 201 healthy newborn infants were randomized to receive either 2.5 pg Hevac B vaccine a t birth [ l , 2 and 14 months in Group I (lOl)] or 5 pg at birth 12 and 14 months in Group I1 (loo)].
Anti-HBsAg responses in the two groups were compared. Passively acquired anti-HBsAg positivity rates at birth were 51.5 and 45.0% in Groups I and 11, respectively. Cumulative anti-HBsAg seroconversion rates in Group I were 12.2,76.6,82.6 and 86.4% at 2 , 4 , 14 and 16 months, while the rates in Group I1 were 2.5, 62.5, 73.7 and 91.0%, showing no significant difference (p > 0.05). Significant difference in seroconversion rates at the 2-month follow-up stage between passively acquired anti-HBsAg-negative and -positive groups was observed (11.9 vs. 2.6%). Significant rise in anti-HBsAg titer at 16 months following the booster at 14 months was noted: 36.4 mIU per ml before, 546.4 mIU per ml after in Group I and 25.3 mIU per ml before, 782.6 mIU per ml after in Group II. The booster, 12 months after the primary vaccination series, is therefore considered imperative for maximum effectiveness of hepatitis B active immunization. Although the present programs of unselective vaccination with modified dose schedules were ineffective for lowering the number of persistent HBsAg carriers for the high-risk newborn infants exposed to HBsAg-and HBeAg-positive mothers, and the high-risk group infants were not excluded in this study, the overall effectiveness of these programs is considered comparable to that of the currently recommended standard dose schedule for immunization of low-risk newborn infants.
Perinatal transmission of hepatitis B virus (HBV)
from carrier mothers to their infants and horizontal transmission of HBV during early life are the most important routes, resulting in the carrier skate of HBV or persistent HBV infection, since HBsAg persistence is inversely related to the age of aquisition of infection (1- 6). It has been shown that persistent hepatitis B surface