AIM:Hepatitis B surface antigen(HBsAg)mutant of hepatitisB virus(HBV)is one of the important factors that result inimmune escape and cause failure of immunization.In thisstudy we reported and characterized a novel HBV mutantwith A-to-G at nt551 and intended to provide theoreticaldata for prevention of HBV infection in China.METHODS:A methodology comprising polymerase chainreaction(PCR)amplifying,M13 bacteriophage cloning andnucleotide sequencing was used to analyze the sera of thepediatric patient who was hepatitis B(HB)immune failure.Expression plasmids containing the mutant S gene and awild-type(adr)S gene were constructed respectively andthe recombinant HBsAg were expressed in COS-7 cells underthe regulation of SV40 early promoter.The recombinantproteins were investigated for their immunological reactivitywith different monoclonal antibodies(mAb)against‘a’determinant and vaccine-raised human neutralizingantibodies.RESULTS:It was found that there was a new point mutationat nt551 of the HBV(adr)genome from A to G,leading to asubstitution of methionine(Met)to valine(Val)at position133 in the‘a’determinant of HBsAg.Compared to the wild-type HBsAg,the binding activity of the muant HBsAg tomAbs(A6,All and $17)and to vaccine-raised human anti-hepatitis B surface antibody(anti-HBs)decreased significantly.CONCLUSION:According to the facts that the patient hasbeen immunized with HB vaccine and that the serum is anti-HBs positive and HBsAg negative,and based on thenucleotide sequence analysis of the mutant HBV S geneand its alteration of antigenicity,the HBV is considered tobe a new vaccine-induced immune escape mutant differentfrom the known ones. AIM: Hepatitis B surface antigen (HBsAg) mutant of hepatitis B virus (HBV) is one of the important factors that result inimmune escape and cause failure of immunization. In this study we reported and characterized a novel HBV mutant with A-to-G at nt 551 and intended to provide theoretical data for prevention of HBV infection in China. METHODS: A method comprising polymerase chain reaction (PCR) amplifying, M13 bacteriophage cloning andnucleotide sequencing was used to analyze the sera of thepediatric patient who was hepatitis B (HB) immune failure. Expression plasmids containing the mutant S gene and awild-type (adr) S gene were constructed respectively and the recombinant HBsAg were expressed in COS-7 cells underthe regulation of SV40 early promoter. recombinant proteins were investigated for their immunological reactivity with different monoclonal antibodies (mAb) against ’ a’determinant and vaccine-raised human neutralizing antibodies .RESULTS: It was found that there was a new point mutationat nt551 of the HBV (adr) genome from A to G, leading to asubstitution of methionine (Met) to valine (Val) at position133 in the’a’determinant of HBsAg.Compared to the wild-type HBsAg, the binding activity of the muant HBsAg tomAbs (A6, All and $ 17) and to vaccine-raised human anti-hepatitis B surface antibody (anti-HBs) decreased significantly. CONCLUSION: According to the facts that the patient hasbeen immunized with HB vaccine and that the serum is anti- HBs positive and HBsAg negative, and based on thenucleotide sequence analysis of the mutant HBV S gene and its alteration of antigenicity, the HBV is considered to be new vaccine-induced immune escape mutant differentfrom the known ones.