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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Ruminant Diseases and Immunology Research » Research » Publications at this Location » Publication #271161
Title: Mechanisms regulating immunity and disease severity following high and low virulence BVDV type 2 infection in neonatal calves

Author
item McGill, Jodi
item SCHAUT, R - Iowa State University
item Neill, John
item Ridpath, Julia
item Sacco, Randy

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 9/12/2011
Publication Date: 11/17/2011
Citation: McGill, J.L., Schaut, R.G., Neill, J.D., Ridpath, J.F., Sacco, R.E. 2011. Mechanisms regulating immunity and disease severity following high and low virulence BVDV type 2 infection in neonatal calves [abstract]. In: Proceedings of the U.S. Bovine Viral Diarrhea Virus Symposium, November 17-18, 2011, San Diego, California. p. 67.

Interpretive Summary:

Technical Abstract: Acute bovine viral diarrhea virus (BVDV) infection can result in a range of disease outcomes from subclinical in the case of low virulence (LV) strains, to anorexia, fever, bloody diarrhea, and death in cases of severe acute disease. Despite the significant range of clinical disease severity, it remains unclear how virus-host interactions and the subsequent immune response differs between strains of high virulence (HV) and LV and how these mechanisms contribute to disease outcome. To this end, the objective of this study was to characterize differences in immune parameters between HV and LV strains of BVDV type-2 in an in vivo setting, and to elucidate the mechanisms by which these changes translate to differences in disease severity. In a series of three individual experiments, a total of 21 clinically healthy, colostrum-deprived, male Holstein-Friesian calves, ages 2 to 5 weeks old, were randomly assigned to three groups. Six calves were infected with BVDV type-2 strain RS886, a LV strain; 8 calves were infected with BVDV type-2 strain 1373, a HV strain; 7 calves served as uninfected control animals. Calves were assessed daily for rectal temperature and peripheral blood samples were collected every other day starting on day-2 post infection (p.i.). These samples were used for BVDV isolation, serum neutralization, and to assess numbers of circulating peripheral blood populations. BVDV infection with both HV and LV strains resulted in a significant reduction in circulating lymphocyte frequencies and numbers. This reduction was most severe and prolonged in animals infected with the HV virus, becoming apparent as early as day 2 p.i., and remaining sustained through the course of the experiment. Interestingly, the CD4 and CD8 alphabeta T cells were effected most rapidly, with HV infected calves showing a nearly 50% reduction by day 4 p.i. B cells and gammadelta T cells followed more delayed kinetics in their loss from circulation, with HV calves showing an approximate 50% loss occurring at day 8-10 p.i. The kinetics of lymphocyte subset loss from the LV calves followed a similar trend; however, the overall magnitude of this loss was less pronounced. Interestingly, numbers of circulating monocytes remained relatively stable throughout the course of both the HV and LV infection, suggesting this cell type may be more resistant to the depleting effects of the virus. HV BVDV infection causes a significant and rapid loss of circulating lymphocytes from the blood that appears more pronounced than that observed in LV BVDV infected animals. Alphabeta T cells appear to be rapidly and severely effected by the virus, while other lymphoid subsets appear more resistant. Future experiments will be aimed at determining the mechanism contributing to the loss of lymphocytes from circulation, and how these immune parameters contribute to differences between HV and LV BVDV infection.