The response to ubiquitous virus infections (A hypothesis)

The human innate anti-A isoagglutinin activity, expressed by polyreactive IgM, is serologically identical to the anti-A activity of C57BL/10 mice and is inhibited by <em>Helix pomatia</em>- and/or Tn-reactive ovarian glycolipids from these animals, which no longer produce the anti-A after early ovariectomy. Thus, the human anti-A antibody does not arise in response to A-allelic (genetic) antigenic activity. While the mouse anti-A antibody, produced together with <em>Helix pomatia</em>- and/or Tn-reactive glycolipids in the autologous ovary and mirrors the egg-protecting function of <em>Helix pomatia</em>-reactive anti-Tn hemagglutinin, the human anti-A most likely reflects nothing more than the monitoring of Tn-associated growth processes and can therefore be considered and referred to as anti-Tn antibody. Moreover, if different viral infections may be inhibited by natural and monoclonal anti-A antibodies, regardless of the infected individual’s ABO(H) blood group, it is unlikely that the stimulatory antigenicity is encoded by an A allele; and if additionally, viral serine molecules are essential for viral infections, this antigenicity is most likely a cross-species, mucin-type hybrid <em>O</em>-GalNAcα1-Ser/Thr-R or Tn formation. While a virus infection is thus initiated by hybrid Tn formation, such a formation also occurs by different pathways due to altered expression of glycan genes in chronic virus infection or virus-induced cancer, and the antibody responding to it is anti-Tn-specific, identical to the cross-reactive anti-A isoagglutinin, which ultimately represents another anti-Tn antibody version and a potential response to ubiquitous virus infections.