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Thirty-seven patients--aged 2 to 58--with clinical and hematological signs of infectious mononucleosis were studied. Thirty patients gave serologic evidence of Epstein-Barr virus infections; antibodies to viral capsid antigen (VCA) appeared very early (only two seroconversions and 4 cases of increased titer were detected); antibodies to early antigen (EA) occured in 25 patients, but only 9 had high titers; antibodies to nuclear antigen (EBNA) appeared late in the course of the disease. VCA-specific IgM antibodies occurred in 25 cases (they usually disappeared during the 2nd month). The transforming EB virus was found in the saliva of the 2 patients where we looked for it. Heterophile antibody responses occured in only 17 patients; among children about half of them had a positive Paul-Bunnell-Davidsohn test. After the age of 40 (3 cases) heterophile antibodies were no longer found. Three patients had another recent viral infection at the same time as the primary EBV infection (two cases of rubella, one case of adenovirus infection). Of the remaining 7 patients (having either no antibodies to EBV or antibodies of past infection), 2 had cytomegalovirus infections and one rubella.

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When AKR mice are irradiated with a sub-lethal dose (4 times 175 R), thymic lymphosarcomas (L.S.) occur earlier than in controls. This accelerated leukaemogenesis is not inhibited by syngenic restoration with bone marrow cells (BM). Using the AKR/T1ALD substrain which bears 38 chromosomes with 1 metacentric markers, it has been shown that AKR radio-chimaeras restored by T1ALD BM developed two kinds of L.S. : (i) early (radiation-induced) L.S. originating mainly from host cells surviving irradiation and (ii) late L.S from donor cells. The present experiments were investigate the potential influence of normal allogenic thymic cells, with or without syngeneic B.M., on the incidence, latency and origin of LS appearing in irradiated AKR recipients. Adding C3H allogenic thymic cells to syngenic B.M. increases the percentage of early L.S. whose latencies are unchanged. Besides, when C3H thymic cells are injected to irradiated controls without syngenic B.M. cells, L.S. are seen to occurr significantly earlier than in just the irradiated animals alone. In radio-chimaeras restored by allogenic thymic cells and syngenic B.M., except in one case, all the L.S. were seen to originate from B.M. cells. The interpretation of these results depends on the possible role of allogenic thymic cells on host cells surviving the irradiation, or the exogeneous B.M. In the first case, allogenic thymocytes could induce a graft versus host reaction increasing the post-irradiation depletion of lymphoid system and hastening thymic endoregeneration which is supposed to be the first step towards leukaemogenesis. The second hypothesis, which seems the most likely, would be that C1H thymic cells could selectively act on host cells surviving irradiation and enhance the differentiation of haemopoietic precursors at the expense of the lymphoid cells. Alternatively the thymic cells may co-operate with exogenic B.M., and stimulate their differentiation thus triggering them out of a stage whereby they could become a selective target for the Gross virus.

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Luekaemogenesis and repopulation of the lymphoid system have been studied in sub-lethally irradiated (c3h x akr/t1ald) f1 hybrids which have been restored with parental Bone Marrow (BM) cells with or without thymic cells. The metacentric marker of the T1ALD sub-strain made it possible to identify the host or donor orgin of leukaemias. Leukaemias occur either in the thymuc (lymphosarcomas) or in the other lymphoid tissues (extra-thymic leukaemias). After irradiation, the precentage of lymphosarcomas increases from 5 to 95%. The rate of leukaemias in hybrids which have been restored only with BM cells is 55, 56 and 100% respectively depending on the origin of BM: syngenic, C3H and AKR. In this last group 75% of the lymphosarcomas originate from donor cells. The inhibitory efficiency of the three kinds of BM on luekaemogenesis seems to be related to their respective abilities to spontaneous malignant transformation. When AKR or C3H thymic cells are injected together with BM cells, leukaemogenesis is altered. The effect is indirect as these cells are not actually concerned by the malignant transformation. The percentage of LS is significantly reduced and the mean survival improved in hybrids restored with C3H thymic, mixed AKR or C3H BM cells. AKR thymic cells are less efficient. In both cases, the percentage of extra thymic leukaemias increases at the expense of lymphosarcomas. Thymic cells do not change the kinetics of repopulation in thymus and lymph-node by the BM cells, except when C3H thymic cells are mixed with T1ALD BM cells; in this case, the lymph-node repopulation is temporarily enhanced. Different hypotheses might explain the effect of thymic cells on leukaemogenesis: enhanced recovery of the postirradiation immunological deficiency, transfer of virus by the AKR thymic cells, and more probably influence of the thymic cells on the maturation or/and differentiation of the lymphoid cells.

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