Submitted to: Viral Immunology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 9/15/2003
Publication Date: 3/1/2004
Citation: Endsley, J.J., Ridpath, J.F., Neill, J.D., Roth, J.A. 2004. Induction of T lymphocytes specific for bovine viral diarrhea virus in calves with maternal antibody. Viral Immunology. 17(1):13-23. Interpretive Summary: The body has two systems to fight off infections. One is the humoral immune system. It is based on the production of proteins that are released into the blood stream. These proteins, called antibodies, bind to disease organisms and prevent them from infecting tissues. The other system is called the cell mediated immune system. It is based on cells (T lymphocytes) that engulf and destroy disease organisms. The activity o the humoral immune system is much easier to measure than the activity of the cell mediated immune system, so measurements of the body's ability to fight off infections is usually determined by the activity of the humoral immune system. This has led to the practice of evaluating vaccines based on their ability to get a response from the humoral immune system. However, it has been suggested that vaccines that cause a response by the humoral system but not the cell mediated system may not work very well. In nthis study we used a model (calves fed high levels of maternal antibodies) that allowed us to tell the difference between protection that was provided by the humoral immune system and protection that was provided by the cell mediated system. We found that the cell mediated system did not require the humoral immune system to prevent disease. These findings suggest that we should change the way we evaluate and license vaccines.
Technical Abstract: This study examined protection from acute disease due to cellular immune response in the absence of measurable humoral immune response. Calves (n=12) fed colostrum with a high titer against bovine viral diarrhea virus (BVDV) for 48 hrs postpartum developed high serum antibody (ab) levels due to uptake of ab from colostrum. Six calves were exposed to a virulent BVDV Vat 1-4 weeks of age when serum ab levels were high. These calves did not become clinically ill or have an increase in serum ab levels. All calves were challenged with BVDV at 7-9 months when serum ab titers had declined to undetectable levels. Serum ab titers of calves exposed to BVDV following colostrum ingestion declined at a similar rate to colostrum fed calves that were not exposed to virus. BVDV specific CD4+, CD8+, or T lymphocytes were determined monthly by two-color flow cytometry, using CD25 as an activation marker. Calves exposed to BVDV following colostrum ingestion demonstrated greater activation of CD4+, CD8+, and T lymphocyte by in vitro antigen and were protected from subsequent BVDV challenge compared to non-exposed animals. This suggests the development of BVDV specific T lymphocytes in the face of maternal antibody, without a detectable humoral response.