Skip to main content
ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #77633


item Lager, Kelly
item Mengeling, William
item Brockmeier, Susan

Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/16/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary: Porcine reproductive and respiratory syndrome (PRRS) is a significant disease of swine which was first recognized about 10 years ago. Since then, the cause of the disease has been identified as the PRRS virus and vaccines for use in pigs have even been developed and sold. In spite of these advances many aspects about the virus-induced disease are still unknown; one of these is a better understanding of the sow's immune response to the PRRS virus. Specifically, does a sow develop a protective immune response and if so, how long would it last? In other words, would the sow be susceptible to another virus infection at a later date? In a previous study we demonstrated that sows develop a protective immune response following exposure to a field isolate of PRRS virus. The goal of the current study was to evaluate how long this protective immunity might last. In the study reported here we were able to demonstrate that protective immunity against the same strain of virus could last for at least 600 days. The results of this study support observations from the field where protective immunity is believed to develop in sows following natural exposure to field virus. Moreover, these results may support the recent licensing of PRRS virus vaccines for use in non-pregnant sows to reduce the incidence of virus-induced reproductive failure.

Technical Abstract: The duration of porcine reproductive and respiratory syndrome virus (PRRSV) homologous immunity was tested and found to last for at least 604 days post primary exposure to virulent virus. Eleven gilts (group A) previously exposed to virulent PRRSV were naturally bred at selected times (143 to 514 days) after primary virus exposure, and on or about gestation day 90 they were oronasally exposed a second time to the same strain of virus. Ten age-matched control sows free of PRRSV antibody from the same source farm (group B) were naturally bred and were oronasally exposed to aliquots of the homologous challenge virus on or about gestation day 90. Nine of the 11 gilts in group A and all animals in group B became pregnant following one breeding cycle. The 2 nonpregnant gilts in group A were each naturally bred during 4 additional estrus cycles and neither one became pregnant. They were exposed to homologous challenge virus 562 and 604 days post primary exposure, respectively. All animals were necropsied 21 days post challenge. Sera and alveolar macrophages from each dam and sera from each fetus were tested for virus. Transplacental infection was detected in 0/9 and 8/10 litters in groups A and B, respectively. Virus was detected in 0/11 and 10/10 of the alveolar macrophage samples collected in groups A and B, respectively. Serum was harvested at selected times throughout the experiment and tested for PRRSV-specific antibody by indirect immunofluorescence microscopy. All gilts in group A were seropositive for the duration of the experiment and all animals in group B seroconverted following exposure to virulent virus. This study demonstrates adult swine can produce a homologous protective immunity following virulent virus exposure which may persist for the production life of the animal.