By Yukiharu Sawada , Deborah Urbanelli , Jana Raskova

Individual human adenoviruses (Ad) ~ vary in their tumorigenic potential in rodents. Group A serotypes induce tumors with high efficiency, while those belonging to the group C are nononcogenic (1). This phenomenon was originally thought to be a reflection of differences in their immunogenicity (2). Isograft transplantation experiments have shown, however, that immunization with both highly oncogenic Adl2 (3, 4) and nononcogenic Ad2 and Ad5 (5) serotypes induces a strong transplantation immunity against tumorigenic Ad-transformed cells. This immunity has been attributed to Ad tumor-specific transplantation antigen (TSTA). The identity of Ad TSTA is unknown. The in vitro reactivity of secondary cytolytic T cells against syngeneic Ad-transformed cells is directed against product(s) dependent on expression in the transformed cells of the Ad early region E1 (6, 7). Examination of a series of mutants of Ad5 for their ability to induce group C A d TSTA in rats revealed that mutants with defects in the region E1 produced significantly lower or no TSTA when compared with Ad2 or Ad5 wild type viruses (5). Adenovirus early gene block E1 contains the region of the viral chromosome that has been shown to be responsible for the transforming activity of the virus (8). It consists of two transcription units E I A and E 1B (9). Effects of immunization with xenogeneic cells transformed with isolated fi'agments of Ad 12 DNA during latency of tumors induced with Ad12 virions suggested that the Ad12 TSTA is a fimction of the left end of the E1B early region (10). This hypothesis was further supported by evidence that cells transformed with a cloned Acc I-H fragment of Adl 2 DNA (0-4.7 map units) failed to elicit secondary cytolytic T cells, which were elicited by cells transformed with the Hind III-G fragment (06.8 map units) of Adl2 DNA (1 1). The TSTA immunity is highly specific: immunization with Ad2 (or Ad5) offers