Bovine immunodeficiency-like virus (BIV) is a bovine lentivirus that has antigenic and genetic homology with the human immunodeficiency virus. Little work has been reported on the effect of BIV infection on bovine immune function. This study was designed to evaluate lymphocyte blastogenesis, mononuclear cell subset numbers, neutrophil function, hematology, and clinical signs in three groups of cattle. These groups were evaluated at 0-2 months post inoculation (PI, Group 1), 4-5 months PI (Group 2), or 19-27 months PI (Group 3). BIV infected animals were inoculated with the R-29 isolate of BIV in tissue culture cells, peripheral blood mononuclear cells from a R-29 infected calf, or a molecular clone of the R-29 isolate. Most inoculated animals seroconverted to BIV by Western immunoblot. BIV was reisolated from most of the animals inoculated. BIV infection was associated with an increase in the lymphocyte blastogenic response to the mitogen phytohemagglutinin in Groups 2 and 3. Neutrophil antibody dependent cell mediated cytotoxicity and neutrophil iodination were decreased (P<0.05) in BIV infected cattle (Groups 2 and 3 and Group 3, respectively). All animals were clinically normal during the evaluation periods. Notable differences were not observed in the other assessments performed. Work with additional BIV isolates and over longer time frames is warranted. Veterinary Immunology and Immunopathology, 36 ( 1993)

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Abstract. An 1 1 -month-old Holstein calf experimentally infected with bovine immunodeficiency-like virus (BIV) developed T-cell lymphosarcoma 5 months postinoculation, concurrent with progressive monocytosis. Tumors were found in the thymus, multiple lymph nodes, and brain. Tumor cells were CD2+, CD4-, CD8-T cells. Infectious BIV could be recovered from splenic tissue and blood mononuclear cells. Bovine leukemia virus was not present. Because this calf was part of an ongoing experiment on the pathogenesis of BIV infection, immune function data were also available both before and after lymphosarcoma developed. Neutrophil and monocyte function were normal, but lymphocyte blastogenesis was enhanced before the development of lymphosarcoma. Follicular hyperplasia in lymphoid tissues was also seen. This case raises the possibility that BIV infection may cause or be associated with some cases of atypical T-cell lymphosarcoma, without evidence of immune suppression at the time of tumor onset.