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Inoculation of ultraviolet (UV)-irradiated adenovirus type 4 (Ad4) led to in vitro transformation of human diploid cells (HDC). Two transformed cell lines could be established: cell line H 1418, from HDC inoculated with the 10(-3) dilution of Ad4 UV-irradiated for 20 min at a distance of 20 cm, co-cultivated with uninfected HDC, and cell line H 1557, from HDC inoculated with the 10(-2) dilution of Ad4 irradiated at the same distance for 12 min. Both transformed cell lines were resistant to superinfection with homologous virus. Virus-specific antigen could be made evident by the indirect immunofluorescence technique in the nuclei of both H 1418 and H 1557 cells.

Mouse Ehrlich ascites carcinoma (EAC) cells proved to be a semipermissive substrate for in vivo cultivation of adenovirus 5 (Ad5) and SV40. The multiplication of SV40 in EAC cells was facilitated by the coinfection with Ad5. As demonstrated by ID and EID reactions, the virus progens isolated at the first passage after the mixed infection of EAC cells with Ad5 and SV40 possess an antigenic mosaic with fractions characteristic of the parental viruses and of the cell substrate in which they had cultivated in vitro and in vivo. The progens gave positive seroneutralization and complement fixation reactions only with antiserum to SV40.

Co-infection of Ehrlich ascites carcinoma (EAC)-bearing mice with Sendai virus and Rous sarcoma virus (RSV) did not result in the formation of complete RSV. Sendai virus could be, however, propagated in this system over 8 serial passages. As demonstrated by immunofluorescence and complement fixation reactions, antigens specific to each virus were synthesized in EAC cells following either single or mixed virus infection. The virus progens also contained antigenic fractions incorporated from the host cell. The incomplete progens synthesized when RSV inoculation preceded that of Sendai virus possessed three polypeptide fractions characteristic of Sendai virus and one RSV-specific fraction.

Neutralizing antibodies to SV-40 were detected in cerebrospinal fluid samples from 16 out of 43 patients with brain tumors and in 6 out of 20 patients with different nonmalignant chronic neurological diseases. The patients' age excluded the correlation with a vaccine-associated or occupational contact with SV-40. The results ascertain the occurrence of SV-40 or of an antigenically related virus in the population of Romania.

The presence of complement fixing antibodies to the avian "gs" sarcoma-leukosis antigen is reported in the personnel of five different fowl farms. Seroconversion was observed in the workers from one of the farms, where the initial antibody incidence was very low.

The results of over 13,500 serological reactions performed in about 3,400 human sera collected from patients with various forms of cancer and from apparently healthy subjects have shown that the humoral immune reactivity of cancer patients as regards their viral antibody response is similar to that of apparently healthy subjects (blood donors or workers exposed to the risk of occupational contact with animal tumor viruses). The authors also remark the presence in the population of antibodies to some viruses with oncogenic potential proved so far only for mammals (adenovirus, SV-40, RSV) or to ubiquitous viruses (e.g. herpes virus) whose transforming activity has been demonstrated for several cell types in vitro and is suspected for some human tumors in vivo.

Two serially transmissible tumors (metastatic lymphosarcomas) were induced in the hamster by inoculation of human brain tumor material--tissue homogenate from a malignized fibroma or DNA extracted from a meningioma. SV40 V antigen was made evident by indirect immunofluorescence in 4 out of 18 human tumors, while SV40 T antigen could only be demonstrated in the tumors experimentally induced in hamsters. Antibodies to SV40 T antigen were detected in 12 out of 60 patients with different tumors, in 1 out of 40 blood donors and in 7 out of 18 hamsters carrying experimentally induced tumors.

DNA extracted from SV40-induced hamster sarcoma (SV40--HS DNA) increased the survival length of animals carrying the homologous tumor and--in some cases--inhibited the development of the tumor. The efficacy of the preparation was directly proportional to the number of administrations; it did not necessarily depend on the amount of SV40--HS DNA per dose. SV40 DNA had no favourable effect on the evolution of the SV40-induced tumor, which suggests that viral DNA does not represent the active component of the SV40--HS DNA preparations. Some possible mechanisms of the effect of homologous tumor preparations are discussed.

Antibodies to the avian group-specific "gs" sarcoma-leukosis antigen were made evident by complement fixation reaction in human sera collected from apparently healthy subjects and from patients with different forms of cancer and non-neoplastic diseases. The number of sera investigated was of 2,123. The possible mechanisms that might account for this paraimmune response of the human organism and the prospects of developing prophylactic steps against cancer are discussed.