| Porcine reproductive and respiratory syndrome (PRRS) continues to be the major viral disease of economic consequence to the swine industry in the United States. Pigs persistently respiratory syndrome virus (PRRSV) are the major impediment to the control and elimination of PRRSV within herds. Three experiments are presented in this thesis to address the diagnosis of acute and persistent infections in adult and young animals and to determine the role of viral quasispecies in mediating infections. The purpose of the first study was to; (1) Evaluate the progression of PRRSV infection in non-pregnant breeding age gifts, (2) Determine the effectiveness of routine diagnostic assays for detection of PRRSV (VI and nRT-PCR) and antibodies (IFA, ELISA and SVN) to characterize acute and persistent infections, (3) Evaluate the usefulness of ante-mortem samples (serum and tonsil biopsies) as diagnostic specimens; and (4) Determine the duration of transmission to naive gifts. Two groups of principal gifts (n=5/group) were housed separately and infected with PRRSV strain VR-2332.; In the second study, the goal was to determine the primary site(s) of PRRSV replication prior to the appearance of viremia. Determining the primary and secondary target tissues of this virus will provide crucial information towards our understanding of the acute and persistent pathogenesis of this disease. The objective of this study was to determine the role of lymphoid and non-lymphoid tissue in acute and persistent infections.; The objective of the third study was to investigate the evolution of ORF5 in pigs from 0 to 126 dpi. Three-week old pigs were either mock-inoculated or inoculated with a plaque-purified virus, strain SD 92-23983 and direct PCR products from serum, lung, palatine tonsil and inguinal lymph node were cloned and sequenced from pigs euthanized at intervals from 6 hpi to 126 dpi. Of 622 clones, the most common change was as 33 (21/45 Gly to Ser; 2/45 Gly to Asn). Only two as changes V29 to A and D30 to N were seen in immunoepitope A and 3 aa changes in epitope B two L41 and the other at N44. (Abstract shortened by UMI.)... |
