Genetic potentials (pedigree-estimated breeding value) for milk and for fat were compared in cows grouped according to subclinical stage of bovine leukemia virus infection. Genetic potential for milk production was significantly greater in seropositive cows with persistent lymphocytosis (662 ± 72 kg) and in seropositive hematologically normal cows (554 ± 34 kg) than in seronegative herdmates (418 ± 53 kg). When 305-day twice-daily-milking mature equivalent milk production records for the current lactation were adjusted for genetic potential, bovine leukemia virus-infected cows that were hematologically normal had significantly greater milk production than did seronegative herdmates, suggesting that early bovine leukemia virus infection was positively associated with milk yield. Genetic potential for fat production was significantly greater for cows with persistent lymphocytosis (21 ± 2 kg) than for other seropositive (16 ± 1 kg) and seronegative herdmates (13 ± 2 kg); however, 305-day twice-daily-milking mature equivalent fat production for the current lactation was not significantly different between the groups. Thus, cows with persistent lymphocytosis did not produce fat according to their genetic potential. As an apparent consequence of tendencies for greater milk yield and less fat production, milk fat percentage was significantly reduced in cows with persistent lymphocytosis (3.33 ± 0.09%) and other seropositive cows (3.48 ± 0.05%) relative to seronegative herdmates (3.67 ± 0.07%). These results suggest a need to reevaluate the economic impact of bovine leukemia virus infection on the dairy industry.Bovine leukemia virus (BLV) is a type C retrovirus that causes a chronic B-cell proliferative disease in cattle (1) and is considered an important model for human T-cell leukemia virus type I infection because of many shared molecular and biological features (2, 3). The essential difference between these two oncogenic viruses is that the primary target cell of BLV infection is the B lymphocyte (4).The pathogenesis of BLV infection proceeds in a stepwise fashion. Cattle infected with BLV will produce antibodies to the major BLV envelope glycoprotein (BLV-gpSl) (5), usually followed by the appearance ofantibodies to the viral core protein, p24 (6). Approximately 30% of BLV-infected animals develop a persistent lymphocytosis (PL) (7), which is characterized by a dramatic increase in the percentage and absolute number of B cells in peripheral blood (8, 9). About one-third of the B cells in cattle with PL have BLV provirus (10). The PL stage of BLV infection identifies animals that are at increased risk for developing lymphosarcoma (7), the terminal stage of the disease, and recent studies have shown that susceptibility to B-cell lymphocytosis is under the control of the bovine major histocompatibility complex (11, 12).The economic impact of BLV infection in the United States has been estimated at 44 million dollars per year, primarily because of slaughterhouse condemnation of lymphosarcomatous carcasses (13)...