Quantitative analysis of HBV DNA level and HBeAg titer in hepatitis B surface antigen positive mothers and their babies: HBeAg passage through the placenta and the rate of decay in babies

被引:134
作者
Wang, ZH
Zhang, J
Yang, H
Li, XH
Wen, SJ
Guo, YB
Sun, J
Hou, JL [1 ]
机构
[1] Nanfang Hosp, Med Coll PLA 1, Dept Infect Dis, Guangzhou 510515, Peoples R China
[2] Youan Hosp Infect Dis, Beijing, Peoples R China
关键词
HBeAg quantitation; perinatal transmission; passive-active immunoprophylaxis;
D O I
10.1002/jmv.10493
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
It is well documented that perinatal transmission is the major cause of chronic HBV infection in China. However, the mechanisms,of HBV perinatal transmission are not defined clearly. It is not known whether hepatitis B e antigen can cross the human placenta, and the rate of HBeAg decay in babies with and without HBV breakthrough has not been studied. In this study, HBV serological markers were investigated in 95 hepatitis B surface antigen positive pregnant women. These markers were also studied in the babies at birth and at the age of 6 months and 12 months. The data show that 7.4% (7/95) children were infected with HBV during the first year after birth despite receiving passive-active immunoprophylaxis with hepatitis B immune globulin and hepatitis B vaccine. The surface gene fragment of HBV DNA was cloned and sequenced following PCR amplification in 7 cases of HBsAg positive babies and their mothers. All babies had the same sequences as their mothers, although two babies also had sequences that would produce an amino acid substitution within the "a" determinant. Furthermore, we measured HBeAg titers and HBV DNA levels by using Abbott AxSYM system and LightCycler-based real-time fluorescence quantitative PCR in 54 mother-infant pairs. Thirty-three mothers were HBeAg positive, and 21 mothers were HBeAg negative. Seventy percent (23/33) of neonates from HBeAg-positive mothers were HBeAg positive at birth compared with 0% (0/21) of neonates from HBeAg negative mothers. HBeAg was present at higher titer in the birth sera of the babies with HBV breakthrough than in babies without breakthrough. HBeAg was cleared from the serum in all 19 babies without breakthrough. In 17 of these 19 babies, the HBeAg was cleared within 6 months, and in,two babies clearance took 12 months. The mean serum HBV DNA level in the mothers of the 4 infants with HBV breakthrough was significantly higher than in the mothers of babies who did not become infected. In conclusion, this data suggests that HBeAg can cross the human placenta, and disappears from serum within 6 months in most babies. HBV DNA levels in hepatitis B carrier mothers are associated with the failure of HBIG and vaccine immunization, and the additional influence of transmitted HBeAg cannot be excluded.
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页码:360 / 366
页数:7
相关论文
共 39 条
[1]  
BEASLEY RP, 1983, HEPATOLOGY, V3, P135
[2]   OUTCOME OF PERINATAL HEPATITIS-B VIRUS EXPOSURE IS DEPENDENT ON MATERNAL VIRUS LOAD [J].
BURK, RD ;
HWANG, LY ;
HO, GYF ;
SHAFRITZ, DA ;
BEASLEY, RP .
JOURNAL OF INFECTIOUS DISEASES, 1994, 170 (06) :1418-1423
[3]  
CANHO RD, 1994, J HEPATOL, V20, P483
[4]   VACCINE-INDUCED ESCAPE MUTANT OF HEPATITIS-B VIRUS [J].
CARMAN, WF ;
ZANETTI, AR ;
KARAYIANNIS, P ;
WATERS, J ;
MANZILLO, G ;
TANZI, E ;
ZUCKERMAN, AJ ;
THOMAS, HC .
LANCET, 1990, 336 (8711) :325-329
[5]   FULMINANT REACTIVATION OF HEPATITIS-B DUE TO ENVELOPE PROTEIN MUTANT THAT ESCAPED DETECTION BY MONOCLONAL HBSAG ELISA [J].
CARMAN, WF ;
KORULA, J ;
WALLACE, L ;
MACPHEE, R ;
MIMMS, L ;
DECKER, R .
LANCET, 1995, 345 (8962) :1406-1407
[6]   Identification of hepatitis B surface antigen variants with alterations outside the "a" determinant in immunized Singapore infants [J].
Chong-Jin, O ;
Ning, CW ;
Shiuan, K ;
Keow, LG .
JOURNAL OF INFECTIOUS DISEASES, 1999, 179 (01) :259-263
[7]  
COURSAGET P, 1986, LANCET, V2, P1143
[8]   Ten-year neonatal hepatitis B vaccination program, the Netherlands, 1982-1992: protective efficacy and long-term immunogenicity [J].
delCanho, R ;
Grosheide, PM ;
Mazel, JA ;
Heijtink, RA ;
Hop, WCJ ;
Gerards, LJ ;
deGast, GC ;
Fetter, WPF ;
Zwijneberg, J ;
Schalm, SW .
VACCINE, 1997, 15 (15) :1624-1630
[9]  
Heijtink RA, 1997, J MED VIROL, V53, P282, DOI 10.1002/(SICI)1096-9071(199711)53:3<282::AID-JMV18>3.3.CO
[10]  
2-S