Bovine leukaemia virus (BLV) resides in infected lymphocytes in a latent, repressed state but becomes expressed a few hours after the cells are cultured in vitro. We have identified several conditions and factors affecting the expression of BLV in short-term cultures of naturally infected lymphoid cells. The presence of foetal calf serum in the culture medium greatly stimulates virus expression. This stimulation is not due to cellular proliferation. Transcription of BLV RNA and synthesis of p25 in the cultures of peripheral blood lymphocytes are preceded by a lag period of several hours. Synthesis of BLV p25 in these cultures takes place almost immediately after viral RNA synthesis. Extending previous results, we demonstrate that the plasma and lymphatic fluid of cattle contain factors that suppress and stimulate BLV expression. As a result of systematic examination of several parameters, we have developed reproducible assays for the detection of these factors. It is very likely that their relative concentration in the host is an important determinant of susceptibility and resistance to the development of lymphosarcoma and persistent lymphocytosis in BLVinfected cattle.

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The bovine leukemia virus (BLV), like the human T cell leukemia viruses (HTLV-I and -II), is usually present in its host in a transcriptionally repressed state. However, the viral genome becomes derepressed a few hours after the infected lymphocytes are cultured in vitro. Depending upon the concentrations tested, plasma and lymphatic fluid of BLV-infected cattle have either stimulatory (BSF) or inhibitory (PBB) activity on viral expression in these cultures. These activities can be separated by chromatographic procedures. BSF is either an antiviral antibody or a BLV-induced molecule that binds to IgG. After complete removal of BSF, the PBB activity can be more consistently detected in bovine plasma and lymphatic fluid. PBB activity can also be demonstrated in human plasma. It seems likely that this activity is responsible for the latent state in which BLV, HTLV-I and -II, and human immunodeficiency virus are usually present in their hosts.

The 24-kDa band formed when sera of humans infected with human T cell lymphotropic virus type I (HTLV-1) were reacted with HTLV-I lysates in conventional Western blot (WB) assays was found to be composed of two immunologically unrelated proteins of 24- and 23-kDa. p24, but not p23, carries epitopes shared by the major core proteins of the other known transactivating C-type retroviruses. p23 is unrelated immunologically to the env and tax HTLV-I products but partly cross-reacts with HTLV-I p19. All HTLV-I and simian T cell leukemia virus type I sera tested reacted with p23. Reactivity with p23 was seen with some HTLV-I sera that did not react or reacted weakly with HTLV-I p24. No reactivity with p23 was seen among the 51 human HTLV-II sera tested nor among a large panel of control sera. Because of its type-specificity and strong immunogenicity, p23 provides a reliable serologic marker for the diagnosis of HTLV-I infection and for distinguishing between HTLV-I and -II.