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The objective of this study was to determine the efficacy of a commercially available porcine reproductive and respiratory syndrome virus (PRRSV)-1 modified-live virus (MLV) vaccine against PRRSV-1 and PRRSV-2 challenge in late-term pregnancy gilts. Gilts were vaccinated with the PRRSV-1 MLV vaccine at 4 weeks prior to breeding and then challenged intranasally with PRRSV-1 or PRRSV-2 at 93 days of gestation. After PRRSV-1 challenge, vaccinated pregnant gilts had a significantly longer gestation period, significantly higher numbers of live-born and weaned piglets and a significantly lower number of stillborn piglets at birth compared to unvaccinated pregnant gilts. No significant improvement in reproductive performance was observed between vaccinated and unvaccinated pregnant gilts following PRRSV-2 challenge. Vaccinated pregnant gilts also exhibited a significantly improved reproductive performance after challenge with PRRSV-1 compared to vaccinated pregnant gilts following PRRSV-2 challenge. The PRRSV-1 MLV vaccine was able to reduce PRRSV-1 but not PRRSV-2 viremia in pregnant gilts. Vaccinated gilts also showed a significantly higher number of PRRSV-1-specific IFN-γ-secreting cells (IFN-γ-SC) compared to PRRSV-2-specific IFN-γ-SC. The data presented here suggest that the vaccination of pregnant gilts with a PRRSV-1 MLV vaccine provides good protection against PRRSV-1 but only limited protection against PRRSV-2 challenge in late-term pregnancy gilts based on improvement of reproductive performance, reduction in viremia and induction of IFN-γ-SC.

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The objective of this study was to compare the severity of reproductive failure caused by either a single or a dual infection with porcine reproductive and respiratory syndrome virus (PRRSV)-1 and PRRSV-2 in late-term pregnancy gilts. Pregnant gilts were intranasally administered PRRSV-1, PRRSV-2 or both at 3 weeks before the expected farrowing date (93 days of gestation). Regardless of single and dual infection, PRRSV-infected pregnant gilts experienced premature farrowing (103-109 days of gestation) compared with negative control gilts which carried their pregnancy to full term (114-115 days of gestation). Pregnant gilts infected with only PRRSV-1 had a significantly (p < 0.05) higher number of genomic copies of PRRSV-1 in their blood compared with dually infected gilts. Additionally, stillborn foetuses and live-born piglets from pregnant gilts infected with only PRRSV-1 had a significantly (p < 0.05) higher number of PRRSV-1-positive cells per unit area of tissue sections examined, compared to pregnant gilts dually infected with PRRSV-1 and PRRSV-2. In contrast, pregnant gilts infected with only PRRSV-2 showed no difference in the number of genomic copies of PRRSV-2 compared with dually infected pregnant gilts and there were no significant differences in PRRSV-2-positive cells per unit area in tissues of stillborn foetuses and live-born piglets from pregnant gilts infected with PRRSV-2 only compared with dually infected gilts. Interestingly, even though PRRSV-2 was shown to replicate more efficiently compared with PRRSV-1 in dually infected pregnant gilts, neither PRRSV type was able to exacerbate reproductive failure in pregnant gilts already dually infected with PRRSV-1 and PRRSV-2. Our results suggest that the severity of reproductive failure is similar between dual (PRRSV-1 and PRRSV-2) and single infection (PRRSV-1 or PRRSV-2).