Objective Maternal hepatitis B virus (HBV) infection can cause fetal infection in utero, but itsmechanism is not clear. This paper tried to show the presence of HBV in placental cells exposed to HBV during pregnancy, ...Objective Maternal hepatitis B virus (HBV) infection can cause fetal infection in utero, but itsmechanism is not clear. This paper tried to show the presence of HBV in placental cells exposed to HBV during pregnancy, the risk factors of intrauterine infection and to trace the possible transmission route frommother to fetus. Methods: ELISA, PCR and ABC immunohistochemical staining with monoclonal anti-HBsand anti-HBc antibodies were used for detection of HBV infection markers in serum and placenta. Case control study was used for analysis of risk factors. Results: The intrauterine infection rate among the infants of101 HBsAg-positive mothers was 7. 9% (8/101 ). The intrauterine infection rate among the infants of maternal HBeAg positive was significantly higher than that of maternal HBeAg negative (X2= 7.22,p＜0.01). HasAg and/or HBcAg were detected in 40 of 101 placentas of HBsAg-positive mothers. The positive rates in cidual cell (DC), trophoblastic cell (TC), villous stromal cell (VSC) and villous capillary endothelial cell(VCEC) were 36. 6% (37/101 ), 28. 7% (29/101 ), 24. 8% (25/101 ) and 11. 9% (12/101), respectively.There was a gradually decrease of HBV infection from maternal side to fetal side of placenta. The Odds ratios(ORs) of HBV intrauterine infections due to infections of TC, VSC and VCEC of placenta barrier were 9. 13,11. 68 and 43. 50, respectively. There was an increasing trend of the ORs from maternal side to fetal side ofplacenta. Conclusions: These data suggested that HBV could infect placenta tissue. The risk factors of HBVintrauterine infection are maternal HBeAg positve and infection of placenta barrier. The transplacental transmission of HBV may be a cellular transfer.展开更多
文摘Objective Maternal hepatitis B virus (HBV) infection can cause fetal infection in utero, but itsmechanism is not clear. This paper tried to show the presence of HBV in placental cells exposed to HBV during pregnancy, the risk factors of intrauterine infection and to trace the possible transmission route frommother to fetus. Methods: ELISA, PCR and ABC immunohistochemical staining with monoclonal anti-HBsand anti-HBc antibodies were used for detection of HBV infection markers in serum and placenta. Case control study was used for analysis of risk factors. Results: The intrauterine infection rate among the infants of101 HBsAg-positive mothers was 7. 9% (8/101 ). The intrauterine infection rate among the infants of maternal HBeAg positive was significantly higher than that of maternal HBeAg negative (X2= 7.22,p＜0.01). HasAg and/or HBcAg were detected in 40 of 101 placentas of HBsAg-positive mothers. The positive rates in cidual cell (DC), trophoblastic cell (TC), villous stromal cell (VSC) and villous capillary endothelial cell(VCEC) were 36. 6% (37/101 ), 28. 7% (29/101 ), 24. 8% (25/101 ) and 11. 9% (12/101), respectively.There was a gradually decrease of HBV infection from maternal side to fetal side of placenta. The Odds ratios(ORs) of HBV intrauterine infections due to infections of TC, VSC and VCEC of placenta barrier were 9. 13,11. 68 and 43. 50, respectively. There was an increasing trend of the ORs from maternal side to fetal side ofplacenta. Conclusions: These data suggested that HBV could infect placenta tissue. The risk factors of HBVintrauterine infection are maternal HBeAg positve and infection of placenta barrier. The transplacental transmission of HBV may be a cellular transfer.
