Porcine reproductive and respiratory syndrome (PRRS) is one of the most challenging subjects of research in veterinary viral immunology, and the immune response against PRRS virus (PRRSV) still is poorly understood. Infected pigs develop a strong and rapid humoral response but these initial antibodies do not confer protection and can even be harmful by mediating an antibody-dependent enhancement of disease. In contrast, development of neutralising antibodies (NAs) is delayed and generation of cell-mediated immune responses, such as PRRSV-specific interferon (IFN)-gamma secreting cells, is initially erratic. In spite of this, induction of strong and rapid NAs and IFN-gamma responses seem to be required for effective vaccination. PRRSV strongly modulates the host's immune responses. The virus inhibits key cytokines, such as IFN-alpha, and may induce regulatory cytokines, such as interleukin (IL)-10. Development of NAs seems to be impaired by the existence of a decoy epitope close to the main neutralisation epitope in glycoprotein 5. This ability to modulate the host immune response probably varies among strains or isolates. The genetic diversity of the virus is very high and it has been shown that this diversity can have serious implications for the development of vaccines, since the immunity induced by one strain may be only partial against a different strain, even within the same genotype. With this panorama, the development of newer and universally efficacious PRRSV vaccines is challenging, but the present state of knowledge allows optimism if collaborative efforts are undertaken in the scientific community.

Porcine reproductive and respiratory syndrome (PRRS) is considered to be one of the most costly diseases affecting intensive pig production worldwide. Control of PRRS is a complex issue and involves a combination of measures including monitoring, diagnosis, biosecurity, herd management, and immunization. In spite of the numerous studies dealing with PRRS virus epidemiology, transmission of the infection is still not fully understood. The present article reviews the current knowledge on PRRSV transmission between and within farm, and the impact of vaccination on virus transmission.

The purpose of this experiment was to study the immune response of pigs during an experimental infection with a European strain of Porcine reproductive and respiratory syndrome virus (PRRSV). Five pigs were challenged intranasally with PRRSV strain VP21 and another five were kept as controls. Clinical course and humoral and cell-mediated responses were monitored for 70 days post-infection (p.i.). Infected pigs developed mild signs at 24 h p.i. Viraemia was detectable by nested RT-PCR until day 14 p.i. Earliest seroconversions (ELISA) were seen by day 7 p.i. (three of five animals) and, by day 14, all inoculated pigs had seroconverted (ELISA and immunoperoxidase monolayer assay). Virus-neutralizing antibodies were undetectable until day 56 p.i. and, by day 70 p.i., two inoculated pigs still were negative. Flow-cytometry assays using peripheral blood mononuclear cells (PBMC) showed an upshift in CD8+ cells (day 7 p.i.) and a downshift of CD21+ cells (days 7 and 28 p.i.). Regarding cell-mediated responses, development of PRRSV-specific gamma interferon-secreting cells (IFN-γ-SC) and interleukin 4-secreting cells (IL4-SC) in PBMC was examined by ELISPOT assay. IFN-γ-SC were not detected significantly until day 14 p.i., whereas, for IL4-SC, no differences between groups were seen. Concurrently with the onset of viraemia and the development of clinical signs, serum haptoglobin levels and interleukin 10 (IL10) in PRRSV-stimulated PBMC-culture supernatants increased significantly. These differences disappeared later on. For IL2, IL4, IL8 or transforming growth factor beta, no differences were seen among groups. These results are compatible with a model in which the immune response does not fully control the outcome of the infection.