This is our Friday rubric: every week a new Science Page from the Bob Morrison’s Swine Health Monitoring Project. The previous editions of the science page are available on our website.
Today’s Science Page is a breakdown of a recent study done by Julia P. Baker, Albert Rovira, and Kimberly VanderWaal of the University of Minnesota, in which they studied PRRSV-2 re-breaks and how the virus changed over time.
Key points:
- Clinical re-breaks of PRRSV on sow farms are a frustrating reality for producers and practitioners and occur despite consistent use of modified live vaccines (MLV).
- 13 re-break events on 12 farms were identified from production and diagnostic data and were analyzed at the whole genome level.
- Numerous amino acid sites on structural proteins were observed to change frequently between the primary and secondary outbreak. This includes sites previously associated with escape from serum neutralization or to be positively selected, and sites known to be accessible to antibodies.
Introduction
Clinical re-breaks of PRRSV on sow farms are a frustrating reality for producers and practitioners. The underlying mechanisms allowing for a single viral variant to persist and cause repeated clinical outbreaks within a herd that should have strong immunity from recent exposure to a highly similar genetic variant (≥%97 homology) are poorly understood. This study systematically identified clinical re-breaks on sow farms and performed whole genome sequencing on viral isolates available from each outbreak event to investigate if specific amino acid site substitutions within structural proteins are associated with re-breaks.
Methods
A United States production system shared abortion counts, vaccination histories, gilt acclimation protocols, and diagnostic data for all sow farms from January 2017 through March 2023. From this dataset, clinical re-breaks were identified within individual farms according to the following criteria: a primary spike in weekly abortion counts above an upper threshold, with concurrent decrease in processing fluid CTs, followed by a second spike of weekly abortion counts above the threshold within 3-12 months, with an ORF5 nucleotide homology of ≥ 97 % with the primary abortion spike. Viral isolates from each abortion outbreak event were sequenced to the whole genome level. The amino acid sequences for the structural proteins were compared for each re-break pair.
Results
13 re-break events from 12 farms met criteria and had samples available. PRRSV variants involved in re-breaks belonged to L1H, L1E, and L1C sublineages. The median ORF5 genetic distance between the re-break pairs was 1.1 % (IQR: 0.54–1.7 %) and the median whole genome genetic distance was 1.82 % (IQR: 0.67–3.62 %). The median number of days between each sample was 213.5 days (IQR: 139.5–230.8). We compared amino acid sequences for each re-break, focusing on the structural proteins. For amino acid sites identified on GP5, several sites were changed in a higher proportion of re-breaks than expected from background variability (Table 1). Intriguingly, 4 of 13 re-break events had no changes on GP5 but numerous changes in other structural proteins. GP2, E, GP3, and GP4 all contained several sites that were substituted in a high proportion of rebreak pairs. Across all structural proteins, most changed sites were in areas accessible to host antibodies (15/22; 68 %). Several GP5 sites (6/8; 75 %) have been associated with escape from antibody neutralization in both in vivo and in vitro experiments (Table 1).
Discussion
Re-break events were identified from several sow farms. Despite close homology across the genomes, there were numerous amino acid sites that changed between the primary and subsequent breaks on individual sow farms. These mutations occurred primarily in antibody accessible regions of the structural proteins and included sites on GP5 associated with immune escape phenotypes in the laboratory. This work addresses the limited understanding of the antigenic importance of all PRRSV structural proteins and supports generating whole genome sequences from PRRSV outbreaks in sow herds.
This study was recently published and is available online and in print from Veterinary Microbiology.
Baker JP, Rovira A, and VanderWaal K. “Repeat Offenders: PRRSV-2 Clinical Re-Breaks from a Whole Genome Perspective.” Veterinary Microbiology 302 (March 1, 2025): 110411. https://doi.org/10.1016/j.vetmic.2025.110411.
References
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5. Kim et al. Veterinary Microbiology 162 (2013) 10–22. https://doi.org/10.1016/j.vetmic.2012.08.005
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