Abstract
In high prevalence settings, mother-to-child transmission is responsible for more than 50% of chronic Hepatitis B Virus (HBV) infections with 1-9% of newborns of HBV-carrying mothers acquiring HBV in early life. Little is known about the routes and cellular mechanisms by which HBV intrauterine transmission occurs. Clinical studies indicate that placental trophoblasts can be infected with HBV. In vitro studies using primary trophoblast and cell lines support this hypothesis. Several cellular parameters, including the differentiation state of the trophoblasts, cytokine secretion, and the surface molecules involved in virus entry, may influence the receptivity of trophoblastic cells to HBV. In HBV-infected trophoblastic cells, a reduction of apoptosis and increased production of antiviral cytokines has been observed, presumably via an HBx antigen-Akt or TLRs-MyD88-NF-kB pathway. Trophoblast HBV infection occurrence involves complex pathological processes with little currently known of the related mechanisms within infected cells. Whilst much focus has been on the placental routes of infection, through trophoblasts in particular, other routes have also been suggested. In this article, we review the models for HBV mother-to-child transmission and discuss the possible mechanisms of HBV intrauterine transmission with particular emphasis upon the involvement of placental trophoblast infection.