Study On The Distribution Of Annexin V And FcγRⅢ In Human Placenta And Their Roles In The HBV Intrauterine Infection

Hepatitis B is still a major epidemic worldwide and has a serious effect on people's life and health. Many studies by immunophathologic and molecular biologic technology confirmed that hepatitis B virus (HBV) could infect the cells of placenta. But little is known about the mechanism of attachment and penetration of HBV-particles into target cells. HBV can be transmitted from pregnant woman to her fetus through the placenta. It is called HBV intrauterine transmission. The rate of HBV intrauterine transmission was 5%~15% in the hepatitis B surface antigen positive mothers. The acquired HBV infection of fetus in gestation was not completely cut off by hepatitis B vaccine and hepatitis B immunoglubin. The intrauterine transmission is the first and important reason for the failure of hepatitis B immunity. The fetus acquired HBV infection by intrauterine transmission would become the virus chronic carriers, may progress to chronic hepatitis and eventually cause cirrhosis and hepatocelluar carcinoma. It has been a serious problem affected the improvement of people's life quality. So the studies on the mechanism of HBV intrauterine transmission have been one of the keys to control the epidemic of hepatitis B.We have explored the risk factors, mechanism and infection time on HBV intrauterine transmission in our department from 1992. Modern epidemiologic, molecular biologic and pathologic technologies have been used. It has studied that the intrauterine infection can occur in the second-trimester pregnancy. But with the continuing of pregnant period the sytotrophoblasts is becoming thiner and in the third-trimester the placenta has stronger penetration. It is easy for the HBV-particles to break through the placenta barrier and so the main timing of infection is possibly in the third-trimester pregnancy. For this reason, the tissues of full term placentae were enrolled in this study. In our department the studies of HBV intrauterine transmission were performed in last decades. Our studies suggested that there might be two pathways on the mechanism of HBV intrauterine transmission, ie, hematogenous transfer and celluar transfer. It was postulated that there appeared to be a "cellular transfer" of HBV from cell to cell in the placenta. Firstly, HBV infected the decidual cells and villi trophoblasts by someway, then infected the villous capillary endothelial cells through cellular transfer, and caused the fetus intrauterine infection eventually. But there is no confirmed conclusion about the mechanism of HBV infection to the placenta! cells. It is studied that the receptor-mediated internalization is a dominating way of virus into the target cells. The research on the mechanism of HBV infection focuses on the interaction of the virus and receptors. HBV is a hepadnavirus. In the studies of hepatocyte infection human annexin V (hAnV) was found to be one of the possible receptors of HBV into the target cells. hAnV plays a key role in the initial step of HBV infection. In this study, the distribution of hAnV in the placenta and the relationship between hAnV and HBV intrauterine transmission were investigated. In addition, antibody-dependant enhancement of infection (ADE) was found in the studies of some virus infection. One of the styles of ADE is that virus conjugated the IgG antibody to be the complex, and internalized into the target cells with the Fc fragment receptor on the surface of cells mediated. The relationship between Fc gamma receptor (FcyR) and HBV intrauterine infection has been explored in our previous studies. In this study, we further investigated the distribution of the transmembrane receptor FcyRIII and at the same time, we investigated the complement C3c to comfirm the existence of HBsAg-anti-HBs-C3c complexes in the infected placental tissues. The role of FcyRIII was further explored in introducing the complexes to penetrate the trophoblasts and result in the HBV intrauterine infection.MATERIALS AND METHODS: 39 full-term placental tissues of HBsAg sero-positive and 4 full-term placental tissues of HBsA...