The effect of molybdenum-induced copper deficiency on acute-phase protein concentrations, superoxide dismutase activity, leukocyte numbers, and lymphocyte proliferation in beef heifers inoculated with bovine herpesvirus-1.

This study was conducted to determine the effect of Cu deficiency on acute-phase protein concentrations, superoxide dismutase activity, leukocyte numbers, and lymphocyte proliferation in heifers inoculated with live bovine herpesvirus-1 (BHV-1). Hereford x Angus heifers were allotted by weight and initial liver Cu concentrations into molybdenum (Mo)-supplemented (n = 6) or control (n = 6) groups. Control heifers were fed a basal diet supplemented with Cu-sulfate to achieve a dietary concentration of 8 ppm of Cu. The Mo-supplemented heifers received the basal diet supplemented with Mo to achieve a dietary Mo:Cu ratio of 2.5:1 and with sulfur at .3% of the diet. All treatments were delivered for 129 d, when heifers were inoculated intranasally with BHV-1. To ensure adequate Cu stores before viral challenge, control heifers were given a cupric glycinate injection on d 100 of treatment. On d 129, Mo-supplemented heifers were considered Cu-deficient (liver Cu = 23.2 and 90.1 ppm for Mo-supplemented and control, respectively). Neutrophils were increased (P < .01) on d 129 in Mo-supplemented heifers. Ceruloplasmin, a copper-dependent acute-phase protein, increased (P < .01) by 48 h after challenge in control but not in Mo-supplemented heifers. Fibrinogen, an acute-phase protein not containing copper, increased by 48 h after challenge in Mo-supplemented but not in control heifers. Erythrocyte superoxide dismutase (SOD) activity was less (P < .05) in Mo-supplemented heifers on d 129. Viral challenge had no effect on SOD activity. Lymphocyte proliferative response to phytohemagglutinin stimulation was greater (P < .01) for Mo-supplemented heifers following BHV-1 challenge. No differences were detected when lymphocytes were stimulated with concanavalin-A or pokeweed mitogens. These data indicate that Cu deficiency alters the acute-phase protein response to viral infection and may affect lymphocyte responsiveness to mitogen stimulation.