Abstract
This study evaluated the efficacy of various vaccination strategies against porcine reproductive and respiratory syndrome virus type 2 (PRRSV-2) in terms of growth performance and immune responses under field conditions at a commercial swine farm in Korea. A total of 80 pigs was randomly assigned to 1 of 4 groups: VacL (modified live vaccine), VacK (inactivated vaccine), VacLK (modified live vaccine followed by an inactivated vaccine), and UnVac (unvaccinated control).
Assessments included clinical signs, blood PRRSV RNA levels, PRRSV-specific interferon-gamma-secreting cells (IFN-γ-SCs), ELISA S/P ratios, neutralizing antibody titers, and growth performance. The VacLK group showed superior growth performance compared with the other groups. At 84 days post-vaccination, blood PRRSV RNA levels were significantly lower in the VacLK group than in the VacL, VacK, and UnVac groups, whereas PRRSV-specific IFN-γ-SCs and ELISA S/P ratios were highest in the VacLK group. These results indicate that a combined vaccination strategy effectively enhanced cell-mediated immune responses, suppressed viral replication, and improved growth performance under field conditions. This study provides valuable evidence supporting optimized PRRSV vaccination strategies for commercial swine production.
Résumé
Cette étude a évalué l’efficacité de différentes stratégies de vaccination contre le virus du syndrome reproducteur et respiratoire porcin de type 2 (VSRRP-2) en termes de performances de croissance et de réponses immunitaires dans un élevage porcin commercial en Corée. Quatre-vingts porcs ont été répartis aléatoirement dans l’un des 4 groupes : VacL (vaccin vivant modifié), VacK (vaccin inactivé), VacLK (vaccin vivant modifié suivi d’un vaccin inactivé) et UnVac (témoin non vacciné).
Les évaluations ont porté sur les signes cliniques, les taux d’ARN du VSRRP dans le sang, les cellules sécrétrices d’interféron gamma spécifiques du VSRRP (IFN-γ-SCs), les rapports S/P (échantillon/positif) en test ELISA, les titres d’anticorps neutralisants et les performances de croissance. Le groupe VacLK a présenté des performances de croissance supérieures à celles des autres groupes. Au jour 84 après la vaccination, les taux d’ARN du VSRRP dans le sang étaient significativement plus faibles dans le groupe VacLK que dans les groupes VacL, VacK et UnVac, tandis que les taux d’IFN-γ-SC spécifiques du VSRRP et les rapports S/P mesurés par ELISA étaient les plus élevés dans le groupe VacLK. Ces résultats indiquent qu’une stratégie de vaccination combinée a efficacement renforcé les réponses immunitaires à médiation cellulaire, supprimé la réplication virale et amélioré les performances de croissance en conditions d’élevage. Cette étude apporte des preuves précieuses en faveur de stratégies de vaccination optimisées contre le VSRRP pour la production porcine commerciale.
(Traduit par Docteur Serge Messier)
Introduction
Among various viral diseases, porcine reproductive and respiratory syndrome (PRRS) is, at the moment, considered a major challenge causing significant economic damage to the global swine industry. PRRS virus (PRRSV) is a positive-sense RNA virus and belongs to the order Nidovirales, family Arteriviridae (1). PRRSV was first identified in the early 1990s, with reports of its discovery and isolation in the Netherlands and the United States, respectively (2,3). Outbreaks of PRRS on farms cause respiratory distress and this is one of the primary causes of significantly increased nursery phase mortality (4), reduced growth rates, impaired digestibility, and decreased feed efficiency in the grower-finisher phase (5).
According to data from the United States, pigs infected with PRRSV from 2000 to 2002 exhibited a reduction in average daily gain (ADG; kg/d) of 0.095 kg, which corresponds to an approximate 25.3% decrease during the nursery phase, and a reduction of 0.091 kg (~12.0%) during the grower-finisher phase. The economic losses attributable to PRRS were estimated at $6.01 per pig during the nursery phase and $7.67 per pig during the grower-finisher phase (6). Further analysis of data from 2005 to 2011 indicated that the total annual economic loss in growing pig herds amounted to $361 855 958 (7). More recent estimates suggest that the annual productivity loss associated with PRRSV in growing pig herds from 2016 to 2020 reached approximately $819 414 866 (8).
In Korea, PRRSV was first isolated in 1993, and the isolate proved to be PRRS type 2 virus (PRRSV-2) (9). PRRSV was already wide-spread in the Korean swine industry; for instance, 89.8% of farms (230 of 256 farms) were confirmed to be positive for PRRSV antibodies in 2001 (10). From 2018 to 2022 in South Korea, PRRSV-2 accounted for 52% of cases (11), and it has been further confirmed that the incidence of PRRSV-2 detection in Korea between 2021 and 2023 was 1.5 times greater than that of PRRSV-1 (12).
To address issues related to PRRSV-2, a commercial PRRSV-2 modified live vaccine was first registered in Korea in 1995, and as of 2025, several companies have developed or introduced PRRSV-2 modified live vaccines and inactivated vaccines.
Following infection through the respiratory tract, PRRSV replicates locally, causing viremia and spreading throughout the body; this viremia plays a critical role in the expression of respiratory clinical symptoms. Efficacy of modified live vaccines can be evaluated by clinical signs, viral load in the blood, interferon-gamma (IFN-γ) responses, lung lesion scores, and viral load in tissues under experimental and field conditions (13).
Inactivated vaccines infrequently induce the production of PRRS-specific antibodies, as measured by enzyme-linked immunosorbent assay (ELISA), or generate virus neutralization titers, as determined through serum neutralization assays (14). In addition, these vaccines seldom provoke CMI responses, as indicated by IFN-γ production (15). Nevertheless, administration of PRRSV inactivated vaccines in swine populations already infected with PRRSV has been shown to enhance both antibody and CMI responses against the virus (14,16). These findings suggest that more comprehensive studies are needed to assess the protective value of inactivated vaccines in herds where PRRSV is present.
Previous research has been carried out predominantly in laboratory environments or within restricted, controlled challenge models (17), with a notable scarcity of investigations that assess efficacy under actual farm conditions. Specifically, empirical field studies examining the use of an inactivated vaccine booster following primary immunization with a modified live vaccine against PRRSV-2 remain rarely documented in the scholarly literature. Moreover, there is a lack of comprehensive data concerning immune response metrics and productivity outcomes. Consequently, the present study aims to assess the effectiveness of this vaccination strategy in enhancing immune responses and productivity parameters within operational pig farming settings.
Materials and methods
Farm history
This study was conducted at an experimental farm located in central Korea that houses a population of 500 sows. The farm is PRRSV-2 positive and employs a 1-week batch management system. Since 2023, the abortion rate among gestating sows has consistently ranged from 1 to 2%, whereas the farrowing rate has averaged approximately 80%, which is marginally lower than the typical benchmark.
The average mortality rate during the nursery phase (from weaning to 70 d of age) has remained around 5%, and the mortality rate during the grower-finisher phase (from 70 d of age until slaughter) has been approximately 3%. Nonetheless, there have been multiple instances in which mortality rates within particular pig batches surpassed 15%, which demonstrates significant variability in mortality levels.
Timing of herd infection
To ascertain the timing of herd-level PRRSV infection, oral fluid samples were collected from piglets at 7-day intervals from 28 to 70 d of age. These samples were subsequently analyzed using real-time polymerase chain reaction (qPCR) to quantify viral load and determine the onset of infection.
Virus isolation
Lung tissues collected from the farm were homogenized in phosphate-buffered saline (PBS), and the clarified solution was filtered through a 0.22-μm pore size filter membrane (Millipore). The clarified lung homogenate was inoculated onto PRRSV-free porcine alveolar macrophage (PAM) cells at 80% confluency. Following a 60-minute adsorption phase, the supernatant was removed and the cells were washed with PBS. The cells were then maintained under standard culture conditions for 48 h in complete RPMI medium enriched with 10% fetal bovine serum and antimicrobial agents, specifically streptomycin and penicillin.
Virus isolation was confirmed by immunocytochemistry using an FITC antibody (18). Total RNA was then extracted as described in a previous study, and PCR targeting the open reading frame 5 (ORF5) region was carried out (19). PCR amplicons were submitted to Macrogen (Seoul, Korea) for ORF5 sequencing using the Sanger method. Phylogenetic analysis of ORF5 sequences was done using RAxML-HPC under the GTRGAMMA model together with reference PRRSV-2 ORF5 sequences.
Vaccines
Considering the epidemiological dominance of PRRSV-2 in Korea (11,12), both a modified live vaccine (Fostera PRRS, Zoetis, Lincoln, Nebraska, USA) and an inactivated vaccine (SuiShot PRRS, CAVAC, Daejeon, Republic of Korea) were selected, as both vaccines are based on PRRSV-2 isolates.
Experimental design
A total of 80 pigs were utilized in this field trial. From an initial population of 280 pigs aged 28 d, 80 individuals were randomly selected and assigned to 4 distinct groups of 20 pigs each (the VacL, VacK, VacLK, and UnVac), using the function in Microsoft Excel that generates random numbers (Microsoft Corporation, Redmond, Washington, United States). The selection process did not account for differences in sow origin or gender.
Pigs assigned to the VacL group received a single intramuscular injection of the modified live vaccine at 28 d of age (0 d post-vaccination, 0 dpv), administered in the muscle behind the ear. Pigs in the VacK group received a single intramuscular injection of an inactivated vaccine at 49 d of age. Pigs in the VacLK group received 2 intramuscular injections: a modified live vaccine at 28 d of age (0 dpv) and an inactivated vaccine at 49 d of age, both administered in the muscle behind the ear. The UnVac group functioned as the untreated group and was not administered any vaccination. Blood samples were collected at 28 (0 dpv), 84 (56 dpv), 112 (84 dpv), and 147 d of age (119 dpv) for subsequent analysis (Table I).
Table I.
Experimental design.
| Group | 1st vaccination | 2nd vaccination | Number of pigs | |||
|---|---|---|---|---|---|---|
| 1st weighing | 2nd weighing | 3rd weighing | ||||
| 1st serum sample collection | 2nd serum sample collection | 3rd serum sample collection | 4th serum sample collection | |||
| 28 d of age | 49 d of age | 84 d of age | 112 d of age | 147 d of age | ||
|
| ||||||
| VacL | FOSTERA | 20 | ||||
| PRRS 2 mL, IM | ||||||
| VacK | SuiShot PRRS | 20 | ||||
| 2 mL, IM | ||||||
| VacLK | FOSTERA | SuiShot PRRS | 20a | |||
| PRRS 2 mL, IM | 2 mL, IM | |||||
| UnVac | 20b | |||||
One pig in the VacLK group died at 74 d of age from a presumptive cause of digestive problems.
Two pigs in the UnVac group died, one at 84 d of age from a presumptive cause of respiratory problems and the other at 92 d of age from a presumptive cause of digestive problems.
Respiratory clinical observation
Respiratory symptoms observed in individual pigs were documented using a quantitative scoring method ranging on a scale of 0 to 6 reflecting symptom severity. Assessments were conducted at 7-day intervals from 28 to 84 d of age (20). Subsequent measurements were taken at 112 and 147 d of age to assess clinical indicators during the grower-finisher stage.
Growth performance
The body weight of individual pigs was recorded at 28 (0 dpv), 84 (56 dpv), and 147 (119 dpv) days of age. Average daily gain (ADG; grams per pig per day) was calculated and analyzed across 2 intervals: i) from 28 to 84 d, ii) from 84 to 147 d, and iii) from 28 to 147 d. Data pertaining to pigs that died during the study were incorporated into these calculations.
Quantification of PRRSV RNA in blood
Viral ribonucleic acid (RNA) was extracted from blood samples or oral fluid collected at each time point using the phenol-chloroform method. Quantification of PRRSV RNA was performed using the OneStep RT-PCR Master Mix (BioFACT, Daejeon, Republic of Korea). The forward and reverse primers used were 5′-TCCAGATGCC GTTTGTGCTT-3′ and 5′-GACGCCGGACGACAAATG-3′, respectively (21).
To construct the standard curves, fragments of the isolated PRRSV, which correspond to the primer-binding regions, were cloned into the pBHA vector (Bioneer, Daejeon, Korea). Serial dilutions of the recombinant plasmids were subjected to real-time polymerase chain reaction (qPCR) to obtain cycle threshold (Ct) values. These Ct values were used to generate standard curves, from which equations were derived to convert the values to log10 RNA copies per milliliter (21). In addition, samples that tested positive at DPV 28 were subjected to ORF5 sequencing as described for sequence confirmation.
Enzyme-linked immunospot assay
An enzyme-linked immunospot (ELISPOT) assay was carried out to quantify the number of PRRSV-specific IFN-γ-SCs (22). PRRSV-specific IFN-γ-SCs were enumerated from peripheral blood mononuclear cells (PBMCs) using an ELISPOT kit (MABTECH) in accordance with the manufacturer’s protocol. Porcine PBMCs were isolated from 4 to 5 mL of whole blood collected in lithium-heparin tubes using density gradient centrifugation with Ficoll-Paque™ PREMIUM (Cytiva, Marlborough, Massachusetts, USA) (23).
Briefly, 5 × 105 PBMCs were seeded into 96-well microplates precoated with a swine-specific IFN-γ capture antibody (10 μg/mL, MABTECH) and subsequently stimulated with the farm-isolated PRRSV diluted in RPMI 1640 medium. Following stimulation, cultures were maintained for a 20-hour period under humidified conditions at 37°C under a gas mixture supplemented by 5% CO2. The assay’s linear response was evaluated at a multiplicities of infection of 0.2 (24). IFN-γ positive spots on the membranes were visualized with streptavidin alkaline phosphatase, analyzed, and counted by microscopic observation. Values were expressed as spot counts of IFN-γ-SCs per 106 PBMCs. All assays were conducted in duplicate to ensure reproducibility.
Serology
Serum samples were analyzed using the commercially available PRRS X3 antibody test (IDEXX, IDEXX Laboratories) for the detection of PRRSV antibodies. Samples were classified as positive for PRRSV antibodies when the sample’s sample-to-positive (S/P) ratio equaled or exceeded 0.4, in accordance with the manufacturer’s guidelines. Serum samples were also evaluated using a serum virus neutralization (SVN) assay against the farm-isolated PRRSV, employing modified protocols based on previous studies (25,26). Prior to testing, serum samples underwent heat inactivation at 56°C for 45 min. Each serum was serially diluted twofold using Dulbecco’s Modified Eagle’s Medium (Sigma-Aldrich, St. Louis, Missouri, USA) with 10% Fetal Bovine Serum (FBS) (Sigma-Aldrich) added, 20 mM L-glutamine, and an antibiotic-antimycotic mixture (Sigma-Aldrich).
Subsequently, 100 μL portions of each serum dilution were combined in a 1:1 ratio with farm-isolated PRRSV at a concentration of 1 × 103 TCID50/mL. The mixtures were incubated at 37°C for 60 min prior to application to confluent MARC-145 cell monolayers cultured in 96-well microplates. The MARC-145 cells were maintained under 200 μL consisting of RPMI medium with 10% FBS added. The cultures were incubated at 37°C under 5% CO2 for a period of 7 d, during which cytopathic effects were monitored and recorded daily. Back titration of the viral inoculum was carried out to confirm the virus titer. The threshold for a positive SVN result was defined as a serum dilution titer of ≥ 2.0.
Statistical analysis
Data obtained from real-time PCR and SVN assays were logtransformed (base-10 and base-2, respectively) to reduce variance heterogeneity. The Shapiro-Wilk test was applied to numerical data, including clinical scores, body weight, viral titers, and immunological parameters, to assess normality. When data met the assumption of normality, differences among groups were analyzed using a 1-way analysis of variance (ANOVA), subsequently followed by Duncan’s post-hoc test to conduct multiple comparisons. For datasets that did not satisfy the normality assumption, the Kruskal-Wallis test was used, and subsequent pairwise comparisons were carried out using post-hoc testing with Holm-Bonferroni adjustment. SPSS software (SPSS, release 29.0; SPSS, Chicago, Illinois, USA) was used for all statistical analyses. The data were expressed as the mean ± standard error of the mean (SEM), and statistical significance was set at P < 0.05.
Results
Farm diagnoses
Analysis of the ORF5 gene from viral strains isolated from the lungs of dead piglets prior to the start of the study revealed that the virus responsible for recurrent infections was PRRSV-2.
RNA was isolated from the oral fluid samples immediately prior to the study’s commencement and subsequently analyzed using real-time PCR to quantify viral load and determine the onset of infection. (Figure 1). A marked increase in viral load was observed between 49 and 56 d of age.
Figure 1.
RNA genomic copies/mL were analyzed at 7-day intervals from 28 to 70 d of age, with the first measurement performed immediately prior to the start of the study, to determine the timing of herd infection.
Respiratory clinical observation
At 56 dpv, respiratory clinical scores were significantly higher in the UnVac group compared to the VacL, VacK, and VacLK groups (P < 0.05). No significant differences in respiratory clinical scores were observed among the 4 groups (VacL, VacK, VacLK, and UnVac) from 0 to 49 dpv; however, an increase in respiratory symptoms was noted from 35 to 56 dpv (Figure 2).
Figure 2.
Mean respiratory clinical scores among 4 groups: VacL (
), VacK (
), VacLK (
) and UnVac (
). Distinct superscript notations (a, b, and c) denote statistically significant differences (P < 0.05) among the 4 groups.
Quantification of PRRSV RNA in blood
The PRRSV genomic copy numbers in the VacLK group were significantly lower than those observed in the VacL, VacK, and UnVac groups (P < 0.05) at 84 dpv (Figure 3). Although the decrease in PRRSV genomic copies from 56 dpv to 119 dpv across all groups did not reach statistical significance, a progressive decrease was evident. ORF5 sequence analysis of the DPV 28-positive samples revealed approximately 87% sequence similarity to the vaccine strain P129 (GenBank no. AF494042), confirming that the detected virus was not the vaccine strain but a circulating field strain.
Figure 3.
Average genomic copy number of PRRSV RNA in blood samples among 4 groups: VacL (
), VacK (
), VacLK (
) and UnVac (
). Distinct superscript notations (a, b, and c) denote statistically significant differences (P < 0.05) among the 4 groups.
Enzyme-linked immunospot assay
At 84 dpv, the quantity of PRRSV-specific IFN-γ-SCs in the VacLK group was significantly higher than the levels in the VacL, VacK, and UnVac groups (P < 0.05) (Figure 4). Although statistical significance was not achieved, the observed effect suggested that the numbers of IFN-γ-SCs in the VacLK, VacK, and UnVac groups tended to exhibit a continued increase up to 84 dpv, followed by a subsequent decline. In contrast, the VacL group demonstrated an increase in IFN-γ-SCs up to 56 dpv, after which a decrease was noted.
Figure 4.
The frequency of PRRSV-specific IFN-γ-secreting cells (IFN-γ-SCs) was assessed across the VacL (
), VacK (
), VacLK (
) and UnVac (
) groups. Distinct superscript notations (a, b, and c) denote statistically significant differences (P < 0.05) among the 4 groups, whereas groups bearing the same letter do not exhibit significant differences.
Serology
The ELISA S/P ratio in the VacLK group was significantly higher than those of the VacL, VacK, and UnVac groups (P < 0.05) at 84 dpv (Figure 5). The mean neutralizing antibody titers did not exhibit statistically significant differences among the VacL, VacK, VacLK, and UnVac groups up to 119 dpv.
Figure 5.
The mean levels of PRRSV antibodies were evaluated among the VacL (
), VacK (
), VacLK (
) and UnVac (
) groups. Statistically significant differences (P < 0.05) among the groups are indicated by distinct superscript letters (a, b, and c).
Growth performance
At 0 dpv, no appreciable differences were evident in mean body weight across the VacL (7.61 ± 0.77 kg), VacK (7.33 ± 0.46 kg), VacLK (7.28 ± 0.83 kg), and UnVac (7.55 ± 0.65 kg) groups. By 56 dpv, the VacLK group exhibited a significantly greater average body weight (30.58 ± 4.74 kg) compared to the VacL (29.85 ± 4.30 kg), VacK (27.60 ± 2.63 kg), and UnVac (28.82 ± 3.47 kg) groups (P < 0.05). In addition, both the VacL and UnVac groups demonstrated significantly higher mean weights relative to the VacK group (P < 0.05), although, no appreciable difference was detected between the VacL and UnVac groups.
At 119 dpv, the VacLK group maintained a significantly higher average body weight (95.23 ± 7.46 kg) than the VacL (91.04 ± 6.14 kg), VacK (87.30 ± 7.37 kg), and UnVac (85.57 ± 9.67 kg) groups (P < 0.05). Furthermore, the VacL group showed a significantly greater mean body weight compared to both the VacK and UnVac groups (P < 0.05), whereas no appreciable difference was determined between the VacK and UnVac groups (Figure 6).
Figure 6.
The average body weight was assessed across the VacL (
), VacK (
), VacLK (
) and UnVac (
) groups. Statistically significant differences among groups (P < 0.05) are denoted by different superscript letters (a, b, and c).
From 28 to 84 d of age, the ADG of the VacLK group (546 ± 85 g) was significantly greater than that of the VacL group (533 ± 77 g), the VacK group (493 ± 47 g), and the UnVac group (515 ± 62 g) (P < 0.05). In addition, both the VacL and UnVac groups exhibited significantly higher ADG values compared to the VacK group (P < 0.05), although no statistically appreciable difference was detected between the VacL and UnVac groups.
During the period from 84 to 147 d of age, the VacLK group demonstrated a significantly higher ADG (1005 ± 59 g) relative to the VacL group (959 ± 50 g), the VacK group (948 ± 79 g), and the UnVac group (875 ± 133 g) (P < 0.05). Furthermore, the VacL group showed a significantly greater ADG than both the VacK and UnVac groups (P < 0.05), whereas no appreciable difference was observed between the VacK and UnVac groups. Considering the entire interval from 28 to 147 d of age, the overall ADG of the VacLK group (736 ± 58 g) was significantly higher than that of the VacL group (700 ± 46 g), the VacK group (672 ± 59 g), and the UnVac group (653 ± 79 g) (P < 0.05). The VacL group also exhibited a significantly greater ADG than the VacK and UnVac groups (P < 0.05), and the VacK group had a significantly higher ADG than the UnVac group (P < 0.05) (Figure 7).
Figure 7.
The average daily gain (ADG; grams per pig per day) was evaluated among the VacL (
), VacK (
), VacLK (
) and UnVac (
) groups. Statistically significant differences between these groups (P < 0.05) are indicated by distinct superscript letters (a, b, c, and d).
Mortality and pathological findings
PRRSV was detected in the lungs of the dead pigs. However, the number of dead pigs was too small to demonstrate a statistical difference among groups. Interstitial pneumonia was observed in all dead pigs, but the lesions were not severe enough to fully explain the cause of death (Supplementary Figure 1; available online from Supplementary Materials). These results suggest that PRRSV may have contributed to mortality; however, mortality was likely influenced by multiple factors, including possible co-infections or other causes.
Discussion
This study assessed the impact of various vaccination protocols using modified live and inactivated vaccines on the clinical signs, immune responses, and growth performance of pigs under field conditions. The findings demonstrate that the PRRS vaccination prime-boost approach (VacLK) provides better protection for growing pigs than single (VacL or VacK) or no vaccination (UnVac) in PRRSV-positive herds.
In this study, the prime-boost regimen (VacLK) demonstrated superior field efficacy, as evidenced by significantly lower viremia levels and clinical scores compared to the other groups. Furthermore, this group achieved the highest growth performance, characterized by significant improvements in body weight and average daily gain. Theoretically, a negative correlation exists between PRRSV viral load and weight gain, suggesting that lower viremia levels may be directly associated with enhanced growth performance in infected pigs (27). These results suggest that the combined benefits of the prime-boost approach promote faster viral clearance and alleviate disease severity, ultimately enhancing overall productivity in PRRSV-positive herds.
In the prime-boost regimen, neutralizing antibody titers did not exhibit significant differences among the groups, which could be attributed to a low sampling frequency and variable natural infection timing that may have hindered the capture of a complete kinetic profile. Nevertheless, the ELISA S/P ratio was found to be significantly higher in this regimen, reflecting a more robust humoral response (28). Although elevated concentrations of neutralizing antibodies in the bloodstream have been shown to correlate with decreased viremia and the inhibition of PRRSV infection (29), it should be noted that ELISA antibody levels do not necessarily correlate with protective immunity (30).
The significant elevation of PRRSV-specific IFN-γ-SCs reflects a strong CMI response, presumably driven by the booster immunization strategy. Previous studies have demonstrated that CMI is a critical factor in PRRSV infection (31,32) and contributes to protective responses (33). In field settings, the observed increase in CMI, as indicated by the increased frequency of IFN-γ-SCs, is thought to be a more direct indicator of protection against PRRSV, mirroring the findings of studies that emphasize the importance of CMI under field conditions (34).
In support of these findings, a laboratory challenge study using a prime-boost strategy comprising modified live vaccine followed by inactivated vaccine demonstrated reduced clinical signs accompanied by a more rapid CMI response (35). Similarly, another experimental prime-boost study reported an increase in cellular immunity, particularly among IFN-γ-producing cells (36). In contrast to modified live vaccine, which preferentially stimulates CD8high T-cells, inactivated vaccine is known to induce both CD4+CD8int+ and CD8high T-cell responses. The CD4+CD8int+ population, which represents the double-positive T-cells that emerge after PRRSV infection, is often regarded as a marker of memory T-cells (37). Consequently, the reduced clinical signs and improved growth performance observed in the combination vaccination group in the present study may have been associated with prime-boost-induced activation of memory T-cells.
Taken together, the findings of this study align with the concept that the prime-boost vaccination strategy confers superior protection against PRRSV, as evidenced by diminished clinical signs, the combination of reduced viral load and augmented CMI responses particularly at 16 wk of age, and enhanced growth performance. These results substantiate the potential of the prime-boost approach as a more efficacious method for managing PRRSV and enhancing productivity in field settings, particularly on farms where frequent post-weaning PRRSV reinfection is suspected to be the cause of reduced market-to-finish productivity. Furthermore, future studies conducted across diverse farm settings would further enhance the potential to more clearly support the effectiveness of the prime-boost strategy.
Supplementary Information
Acknowledgments
The authors’ research was supported by contract research funds from the Research Institute for Veterinary Science (RIVS) at the College of Veterinary Medicine, Seoul National University and BK21 FOUR Future Veterinary Medicine Leading Education and Research Center.
Funding Statement
The authors’ research was supported by contract research funds from the Research Institute for Veterinary Science (RIVS) at the College of Veterinary Medicine, Seoul National University and BK21 FOUR Future Veterinary Medicine Leading Education and Research Center.
Footnotes
Unpublished supplementary material (Figure 1) is available online from: Supplementary Materials.
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