Receptivity of human choriocarcinoma JEGIII cells and isolated trophoblast cells to hepatitis B virus infection and enhancement by tumor necrosis factor alpha.

Intrauterine infection of the fetus is clearly an important mode of vertical transmission of hepatitis B virus (HBV). The trophoblast layer of the human placenta must be traversed by HBV in order to reach underlying cells and fetal capillaries. Although HBV has been detected in the trophoblast layer in situ, the degree of susceptibility of primary trophoblast cells to direct HBV infection in vitro remains unknown. To determine the receptivity of trophoblast cells to HBV infection and to discover the cellular basis for the molecular mechanism responsible for the passage of HBV from the maternal to the fetal circulation, we infected choriocarcinoma JEGIII cells and primary trophoblast cells with HBV. Our findings suggest that the cells could be reproducibly infected with HBV and that the infective patterns of the isolated trophoblasts and JEGIII cells were remarkably similar. In vitro infection resulted in an intracellular viral DNA and hepatitis B surface antigen signal and the secretion of hepatitis B surface antigen into culture medium. The results suggest that both isolated trophoblast cells and trophoblast-derived choriocarcinoma cells are sensitive to infection with HBV in vitro. In addition, we have found that infection of trophoblast cells and JEGIII cells by HBV was enhanced in the presence of tumor necrosis factor alpha. This supports an additional role for tumor necrosis factor alpha in the entry of HBV into trophoblast cells during pregnancy.