Maternal Fetal Transmission of Human Viruses and their Influence on Tumorigenesis
The maternal-fetal barrier represented by the syncytiotrophoblast was shown to be formed by epigenetically regulated endogeneous retroviruses. This barrier, however, possesses certain plasticity, it can be penetrated by nanoparticles of different size-classes, by methabolites, toxic substances by unidirectional or bidirectional transport enzyme systems, intercellular transport mechanisms and by maternal antibodies, immunocomplexes including virus-antibody complexes by specific receptor cascades.
Bidirectional microchimerism perfuse the fetal organism with maternal cells and the maternal organism with fetal stem cells. Chromosomally integrated viruses (human herpesvirus 6, parvoviruses) latently infected lymphotropic herpesviruses and tumour cells can be present among the microchimeric cells which can survive in the recipient organisms in gradually decreasing number for several decades.
Idiotypic interactions of T-B cells enable a generalization of single antigenic experiences and allow a transgenerational learning of the nascent immune system. The latter function is driven by maternal antibodies which represent a great deal of the mother’s immunological knowledge of the external world of antigens. Therefore, maternal antibodies function as transgenerational messengers.
Bidirectional maternal-fetal transport during pregnancy and long-term survival of cells
Fetal illnesses caused by receptor mediated maternal-fetal transport of autoimmune IgG
Receptor mediated transport of maternal anti-idiotypes may induce fetal TREG cells and fetal IgM
Biological therapy of malignancies of pregnants (monoclonal abs) may cause fetal impairment
Virus transport to the fetal body might result in later impairment of tumour defence mechanisms