The effects of vaccination of sheep with a recombinant vaccinia virus (rVV) expressing the bovine leukaemia virus (BLV) envelope glycoprotein (gp60) were studied by determining BLV titres in peripheral blood leukocytes after vaccination and challenge. The proliferation of BLV was suppressed markedly, not only when rVV was inoculated prior to challenge with BLV, but also when it was inoculated after challenge. These results indicate that vaccination with rVV induces protective immunity that can suppress the growth of BLV in carrier animals. Since rVV induced a strong anti-BLV delayed-type hypersensitivity response without producing detectable levels of binding or neutralizing antibodies, and there was no apparent correlation between the humoral immune response and BLV proliferation, a cell-mediated immune response was assumed to play a major role in protective immunity.

ABSTRACT. Thirty-three cases of enzootic bovine leukosis (EBL) and 14 cases of sporadic bovine leukosis (SBL) were examined by immunohistochemistry using 6 monoclonal antibodies against leukocyte differentiation molecules of bovine leukocytes. There were 17 cases of B-1a cell type, 10 cases of B-1b cell type and 6 cases of B-2 cell type in EBL, and 5 cases originating from B cells (B-2 cell type) and 9 cases originating from immature T cells in SBL. The average age for the EBL cases of B-1a cell type was 8.6 years, B-1b cell type was 6.5 years, and of B-2 cell type was 4.5 years. In cases of SBL, immature T cell type patients were younger than B-2 ce ll type ones. The lymphoma originating from B cells differed from that originating from T cells in morphology. In T cell tumors, the nucleus of tumor cells was round, the edge of the cytoplasm obvious, and tumor cells were sporadically present and proliferated. When compared with T cells, the region among B cells was obscure. But, there was no relation between phenotype and the histologic classification of tumor cells. In EBL, beyond the lymph node, tumors of B-1a and B-1b types had developed in the heart and abomasum, and those of the B-2 type tended to occur in liver. In SBL, B-2 type and T type cells formed tumors in the liver, kidney, thymus, and one case of T-cell type tumor formed on the skin. We would like to propose a new classification of bovine leukosis as EBL, calf type B-cell lymphoma, juvenile T-cell lymphoma and skin type T-cell lymphoma.

Lymphocyte proliferation responses were investigated in sheep and cattle, in which the replication of bovine leukemia virus (BLV) had been known to be suppressed by inoculation with recombinant vaccinia virus (rVV) expressing BLV envelope glycoprotein (gp60). Enhanced lymphocyte proliferation responses were observed in animals inoculated with rVV, regardless of whether they were naive or BLV carriers. These responses were roughly inversely correlated to the growth of BLV in the peripheral blood leukocytes. In contrast, there was no apparent correlation between humoral immune response and BLV growth. Based on these results, it was suggested that rVV rendered its suppressive effect of BLV replication primarily via augmentation of cell-mediated immunity.Bovine leukemia virus (BLV) is a type C retrovirus which causes a malignancy of B-cell lineage termed enzootic bovine leukosis in cattle, and shares biological and pathological properties with human T-lymphotropic leukemia virus types I and II (HTLV-I, -II) (1, 5, 10). Determination of the complete nucleotide sequences of these viruses (16)(17)(18)(19) revealed that the organization of their genes is similar. BLV infection usually occurs horizontally and is characterized by a long latent period. It also induces leukemia in sheep at a high incidence within a relatively short period (7, 13), making sheep a good animal model for research on BLV.An increasing amount of data show that the induction of strong humoral immune response to BLV envelope glycoprotein was able to completely protect naive sheep against BLV infection (8,14). Our knowledge is sparse, however, of the immunological mechanisms controlling the replication of BLV after its infection of an animal. To investigate this, we conducted a series of experiments in sheep 131 7

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