For professionals:

• Newborn from carrier mother becomes to be HBsAg carrier in spite of having received vaccination for HBV.
• A few weeks or months after birth, in the presence of anti-HBs, HBsAg become positive, i.e. infected with HBV.
• The 145th aminoacid group of S gene changed from Glycine to Arginine, caused by point mutation of the nucleotide base of the GGA (Glycine) to AGA (Argine).
• The mutation made it to escape from attack or neutralization by HBIG and/or anti-HBs, followed by infection of mutated strain of HBV.
• Two possibilities have been considered and verified. The first, the mutant strain has already been present in the mother in small number, which proliferates and becomes the prominent strain after suppression of wild type strain by HBIG and vaccine-produced anti-HBs. The second, the mutation occurs due to the vaccination.
• First reported in Italy by Carman (1990), followed by reports by Harrison from Singapore, and Fujii and Okamoto from Japan (1992).
• In Taiwan, mass immunization against HBV has been started since 1984, and it has been suggested that there might be of the emergence of vaccine escape mutant. Actually, Hsu, H.Y., Pediat. Dep. of NTUH, has reported the finding of such mutants in Taiwan 10 years after the implementation of mass vaccination program.
• Hsu, H.Y., reported in 1998 that "Although with universal immunization there was a marked decline in HBsAg carrier rate in children, the prevalence of alpha determinant mutants in carrier children increased significantly from 8 of 103 (7.8%) in 1984 to 10 of 51 (19.6%) in 1989 and 9 of 32 (28.1%) in 1994. In all studied carrier children from these surveys, there was much higher prevalence of alpha determinant mutants in those fully-vaccinated than those unvaccinated".
• The presence of both HBsAg and anti-HBs observed in chronic hepatitis cases is another example of escape mutant of S gene (K. Yamamoto, 1994).
• A fulminant hepatitis caused by pre-core mutation is another example of a variant induced hepatic damage.