Three lymphoblastoid cell lines were established from splenic lymphocytes of a lymphomatous baboon (Papio hamadryas) by co-cultivation of the lymphocytes with X-irradiated cells of marmoset or baboon lymphoblastoid cell cultures; the baboon splenic lymphocytes failed to grow when cultured alone. A herpesvirus, associated with each cell line, was identified by immunofluorescence, molecular hybridization and electron microscopy. Antigenic comparison with Epstein-Barr virus (EBV) showed that the baboon herpesvirus and EBV shared cross-reacting viral capsid antigens (VCA): 20 of 20 (100%) anti-VCA (EBV)-positive human sera and 55 of 62 (89%) baboon sera reacted with the baboon lymphoblastoid cells and baboon sera stained EBV VCA in P3HR-1 and EB-3 cells. No nuclear antigen, as assayed by anti-complement immunofluorescence tests, was detected in baboon lymphoblastoid cells when human or baboon anti-VCA positive sera were used. Baboon anti-VCA-positive sera also failed to stain EBV nuclear antigens (EBNA) in Raji or P3HR-1 cells. Preliminary molecular hybridization studies showed only approximately 40% homology between viral DNA of baboon cell lines and DNA of EBV derived from P3HR-1 cells.

A type-C RNA virus has been isolated from various tissues of a lymphomatous baboon (sp. P hamadryas). Virus isolations were made by co-cultivating baboon cells from the inguinal and mesenteric lymph nodes, testes, kidneys and spleen with cells of canine or human origin. The isolated virus grew in canine, bat, rhesus, and human cells but not in cells of mouse, rat, cat or rabbit origin. The baboon isolate resemble a type-C virus when infected cells were examined by thin section in the electron microscope. In addition, the virus was capable of providing helper function by rescuing and transmitting the Moloney and Kirsten sarcoma virus genome from non-productively transformed cells. Antibody directed against the RD114 virus reverse transcriptase was very effective in inhibiting the baboon virus polymerase while while anti-mouse and woolly type-C virus polymerase antibodies had no significant inhibitory activity. Further analysis by immunodiffusion and competitive radioimmune assay revealed a close immunological relationship between this virus, RD114 and another type-C virus isolated from the placenta of a different species of baboon. Finally, three different classes of interspecies antigenic determinants have been demonstrated in mammalian type-C virus isolated from the placenta of a different species of baboon. Finally, three different classes of interspecies antigenic determinants have been demonstrated in mammalian type-C viruses.

Contrary to earlier established opinion that tumors in monkeys are found rarely, now the large material confirms that monkey tumors are frequent phenomenon. Tumor incidence clearly increases with age. Frequencies of benign and malignant tumors of various locations and histogenesis are slightly different. Tumors of hematopoietic system are the most frequent. Sporadic cases and enzootic outbreaks of lymphomas are described for different kinds of monkeys, including apes, and probably are caused by viruses. Two viruses were isolated by us from sick monkeys - the retrovirus C-type STLV-1 and the herpes virus papio HVP. Inoculation of virus cultures into monkeys and rabbits induces neoplasms. Monkey neoplasms can be induced by exposure to various chemical agents, and by oncogenic and non-oncogenic viruses. There is no strict species specificity of tumor viruses. The role of polyoma viruses in neoplasms etiology is discussed.

The genetic structure of EBV LMP1 alleles isolated from tumor, blood, and throat washing samples of 22 nasopharyngeal carcinoma patients, 17 patients with other non-EBV-related tumors of the oral cavity, and 19 blood donors have been studied in representatives of Central Russia and the Republics of Northern Caucasus, regions which are non-endemic for nasopharyngeal carcinoma. The analysis of the LMP1 alleles collected revealed that they practically matched previously described LMP1 variants; however, some characteristic features were also detected. In particular, the G212S substitution in LMP1 isolates investigated was not observed at all. Tumor samples obtained from nasopharyngeal carcinoma and other tumors of the oral cavity did not differ significantly either in the frequency of "high oncogenic" LMP1 alleles with 10 aa and/or 23 aa deletions (LMP1(China1) and/or LMP1(Med+)), nor in the number of 11 aa repeats and the frequency of 5 aa motif insertions. No differences in the frequency of amino acid substitutions between LMP1 alleles obtained from tumor and throat washing samples of both patient groups were also detected. The data obtained may indicate that in both nasopharyngeal carcinoma patients and patients with other tumors of the oral cavity, the EBV strains with similar LMP1 variants are found to persist. This observation allows us to suggest that in non-endemic areas, EBV strains with any LMP1 alleles can initiate the nasopharyngeal carcinoma development but only in those individuals who have a genetic predisposition to the disease and are subjected to specific environmental, and/or dietary factors present in certain geographic areas.

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