Effects of a porcine reproductive and respiratory syndrome virus infectionon the development of the immune response against pseudorabies virus

Citation
Mgm. De Bruin et al., Effects of a porcine reproductive and respiratory syndrome virus infectionon the development of the immune response against pseudorabies virus, VET IMMUNOL, 76(1-2), 2000, pp. 125-135
Citations number
21
Categorie Soggetti
Veterinary Medicine/Animal Health",Immunology
Journal title
VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY
ISSN journal
01652427 → ACNP
Volume
76
Issue
1-2
Year of publication
2000
Pages
125 - 135
Database
ISI
SICI code
0165-2427(20000831)76:1-2<125:EOAPRA>2.0.ZU;2-F
Abstract
The aim of this study was to investigate the effects of a porcine reproduct ive and respiratory syndrome virus (PRRSV) infection on the development of the immune response after pseudorabies virus (PRV) vaccination in pigs. Pig s were intranasally inoculated with the European PRRSV strain, Lelystad vir us ter Huurne, and were vaccinated intramuscularly with PRV 2 weeks later ( LV-PRV group). Control pigs were vaccinated with PRV only (PRV group). Eigh t weeks after PRV vaccination, pigs from both groups were challenged intran asally with wild-type PRV. We measured the lymphoproliferative, and the cyt olytic responses to PRV of peripheral blood mononuclear cells (PBMC), isola ted from blood samples. In addition, serum samples were examined for antibo dies against PRV and LV. One week after PRV vaccination, PBMC proliferated abundantly to PRV in both groups. However, in the LV-PRV group the lymphopr oliferative response declined after 1 week, whereas, in the PRV group, the lymphoproliferative response was high for 3 weeks and declined thereafter ( P<0.05). After challenge, the lymphoproliferative response was 1 week earli er and was consistently and significantly higher in the PRV group than in t he LV-PRV group. The PRV-specific killing was higher at 3 weeks after PRV v accination and 5 weeks after PRV challenge 19+/-3 and 24+/-6%, respectively , in the PRV group, compared to 7+/-4 and 6+/-9%, respectively, in the LV-P RV group (P<0.05). However, later after vaccination and challenge the cytol ytic response was identical in both groups. The antibody titre against PRV developed equally in both groups. After challenge, no PRV virus was isolate d from both groups. From these results we conclude that, although PRRSV inf ection did cause changes in the time course of the T-lymphocyte response af ter PRV vaccination, PRRSV infection did not inhibit the development of vac cine-induced protection after PRV. (C) 2000 Elsevier Science B.V. All right s reserved.