To determine the phenotype of target cells for bovine leukemia virus (BLV) infection in sheep, we analyzed blood lymphocytes from BLV-infected clinically healthy and leukemic sheep by used of monoclonal antibodies. In clinically healthy and leukemic sheep that were BLV-infected, the blood concentration of T lymphocytes was within normal values, but the number of B lymphocytes was increased in several cases. In addition, the number of blood lymphocytes expressing the BLV antigen correlated well with that of B lymphocytes. Double immunofluorescence staining demonstrated that lymphocytes expressing BLV antigens bore B-cell but not T-cell surface markers. Moreover, neoplastic cells in the lymph nodes of leukemic sheep were stained immunohistochemically with an anti-B monoclonal antibody but not with any of anti-T monoclonal antibody tested, indicating that tumor cells are of B-lymphocyte origin. Collectively, these results show that BLV antigen-positive cells obtained from BLV-infected sheep that have no clinical signs and BLV-induced lymphosarcoma cells belong to the B-lymphocyte lineage.

Animals recovered from viral diseases represent an important model to study the host cellular and humoral immune responses to the etiologic agents. This is particularly important for African swine fever virus (ASFV) infections in which antibodies have little or no virus-neutralizing effect. Pigs surviving experimental infection with the naturally occurring low-virulent, nonhemadsorbing ASFV/NH/P68 (NHV) isolate did, however, exhibit virus-specific T-cell activities, as measured by a variety of assays. A strong virus-induced, antigen-specific blastogenic response was observed only with blood mononuclear cells (BMC) from ASF-recovered swine, whereas cells from recovered and naive swine responded similarly to the mitogens concanavalin A and phytohemagglutinin. The ASFV-induced blastogenesis was dependent on virus dose and on the presence of adherent cells. Blood mononuclear cells cultured with antigenically related hemadsorbing ASFV isolates of different virulence characteristics, the highly virulent L60 isolate and moderately virulent DRII isolate, exhibited a similar magnitude of blastogenesis to cells infected with the low-virulent NHV isolate. Virus-infected cells proved to be an efficient inducer of interleukin-2 (IL-2) activity to cells from recovered swine, but not from naive swine, whereas T-cell-specific lectins induced production of similar amounts of IL-2 activity from cells of naive and recovered swine. Correlated with the appearance of virus-induced IL-2 activity in the culture supernatant was the induction of promiscuous killing in cells exposed to prolonged (7 days) virus stimulation. This lymphokine-activated killing could be induced experimentally early in the virus stimulatory process (3 days) by the addition of exogenous lymphokines to the cultures. It was concluded that swine inoculated with low-virulent ASFV isolates are a useful model for identifying and characterizing ASFV immune mechanisms in vitro. Furthermore, this ASFV model implicates lymphokines as inducers of nonspecific cell-mediated immunity; in fact, lymphokine-activated killer type responses may contribute to recovery from this viral infection. More important, ASFV-specific blastogenic and cytotoxic T-cells are prime candidates for the cells inducing and/or conferring protective immunity against challenge ASFV infection.

Immunodeficiency in neonatal and young pigs was studied in terms of T-cell function. Generalized T-cell deficiency did not exist in young pigs on the basis of the in vitro response of blood mononuclear cells to a polyclonal T-cell mitogen, phytohemmagglutinin. However, immunodeficiency that extended from birth up to 4 weeks, was observed in serum antibody concentration and in vitro proliferative responses of blood mononuclear cells from young pigs exposed to a low antigen dose of a T-cell dependent antigen, egg white lysozyme. The low in vitro proliferative response to lysozyme was not attributable simply to a lack of interleukin-2 production, because supplementation with human interleukin-2 did not enhance the in vitro cellular response. Also, pokeweed mitogen-stimulated B cells from young pigs up to the age of 5 to 6 weeks produced immunoglobulin concentration, which also was not affected by the addition of human interleukin-2 to the in vitro cultures. The blood mononuclear cells obtained from pigs within the first 5 to 6 weeks after birth and incubated with monoclonal antibodies reactive to all T cells (MSA4), helper T cells (74-12-4) or suppressor/cytotoxic T cells (76-2-11) did not yield consistent excess of suppressor/cytotoxic T cells. This observed immunodeficiency cannot be attributed to a simple lack of functional T cells or to an excessive number of suppressor/cytotoxic T cells, but may be a property of the ability of specific T-cell clones to respond t o low concentration of T cell-dependent antigens or may be attributable to the induction of a suppressor T-cell population in response to in vitro stimulation with the polyclonal T-cell-dependent pokeweed mitogen system.

Serum uric acid concentrations were determined in horses known to be carriers of combined immunodeficiency gene(s) and in presumed noncarrier horses. Uric acid concentrations were significantly higher (P < 0.005) in carrier horses than in presumed noncarrier horses. However, there was some overlap in serum uric acid concentrations between carrier and presumed noncarrier horses.