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A major antibody combining site on foot and mouth disease virus (FMDV) serotype O1K has been identified in a predicted surface helix of viral protein 1 (VP1) between amino acid residues 144 and 159. A hexadecapeptide covering this sequence elicits high titers of antibodies that specifically recognize and neutralize FMDV. The high quality of the immune response is attributed to a particularly stable conformation of the antigenic amino acid sequence, which is most likely an alpha‐helix.

A precipitating antigen of bovine leukemia virus was isolated by isoelectric focusing and Sephadex gel filtration. In SDS-polyacrylamide gel electrophoresis it was found to be a homogeneous protein with a relative molecular weight of 69 000 daltons. Because of its relative molecular weight and staining characteristics it was designated as BLV gp69. A protein with the same molecular weight could also be demonstrated in BLV particles. In 34 out of 35 sera from cattle affected by enzootic bovine leukosis antibodies against gp69 were detected, whereas the sera from 197 animals, free of bovine leukosis, did not react in immunodiffusion test.

Cells from a secondary tumor developing at the site of a regressed Moloney sarcoma virus-induced tumor could be passaged in adult STU mice by intramuscular and intraperitoneal inoculation. The tumors induced by these cells, as well as by a cell line derived from it, grew progressively and led to death of the animals between 3 and 7 wk after tumor transplantation. No evidence for production of virus from these cells was obtained or for the presence of viral antigens (p30, gp69/71). From both cell variants, sarcoma virus genome could be rescued by infection with helper virus, resulting in the establishment of a cell line producing focus- and XC plaque-forming virus. The rescued producer cells very frequently also produced tumors which finally grew progressively. The nonproducer cells were not immunogenic, as was demonstrated in cross transplantation tests and in studies for cell-mediated cytotoxicity (CMC) and complement-dependent antibody-mediated cytotoxicity (AMC). The producer cells, however, were demonstrated to possess a strong immunogenicity. The nonproducer cells, though nonimmunogenic, revealed a weak immunosensitivity when used for challenge in the transplantation protection assay or as target cell for the demonstration of AMC and CMC, if the immune response was induced by cells producing the sarcoma-helper virus complex, but not by cells producing only helper virus. The nonproducer cells, as well as their rescued producer derivative, showed a stronger reactivity with cytotoxic antibodies than with cytotoxic cells, whereas the helper virus-producing cell line was comparably suitable as target cell for AMC and CMC. The recurrence of a regressed Moloney sarcoma is assumed to be the result of the occurrence of transformed nonproducer cells escaping immune destruction, and not as a consequence of a depleted immune resistance in the host.