The approach to the problem of oncogenesis of tumorigenic viruses is compared and analyzed from the position of the Altshtein-Vogt hypothesis and from that of the general theory of oncogenesis advanced by the present author. In contrast to the hypothesis of Altshtein-Vogt dealing mainly with the problem of oncogene origin, the general theory of oncogenesis not only defines concretely the origin of the oncogene and the essence of its product, but also makes it possible to understand why, when and how integration of the oncogene with the genome of the cell leads to the transformation of the cell into a benign cell and when into a malignant tumour cell. An analysis of the essence of the "oncogene position effect" from this standpoint shows that an integration, similar in its mechanism but differing in polarity, of the genome of other viruses with the cell genome should lead to the formation of a corresponding antiviral stable (life-long) immunity or also to the emergence of pseudoautoimmune disease of the type caused by "slow" viruses.
A serum agglutinin reactive with red cells in the presence of polycarboxyl groups is reported. It is likely that this represents an additional example of the type of agglutinin previously described as agglutinating red cells in the absence of ionized calcium. Experimental evidence is presented indicating that it is free polycarboxyl groups that potentiate agglutination and that any metal ion, such as calcium, capable of chelating with these groups will prove to be inhibitory.
