ArticleVeterinary research2025
Exploring transcriptomic and genomic differences between susceptible and resistant fetal pigs to maternal PRRSV infection at late gestation.
Article in Veterinary research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Immunopathogenesis and pathological features of NADC34-like PRRSV infection in pregnant sows during late gestation.Veterinary research · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome (PRRS) severely impacts global swine production. While studies have revealed host genetic factors and molecular mechanisms of fetal response to PRRSV infection, the relationship between fetal genotype, thymic transcription and PRRS susceptibility remains unclear. This study integrates genomic and thymic transcriptomic analyses of fetal pigs from a maternal PRRSV-2 challenge model. Fetuses were categorized by susceptibility to PRRS, following maternal inoculation at gestation day 84-86 into four groups: complete resistance (CR), partial resistance (PR), viable susceptible (VS), and meconium-stained susceptible (MS). CR and PR fetuses exhibited 0 or less than 4 viral loads in serum and thymus, respectively, despite maternal exposure, while VS and MS fetuses had high viral loads with MS showing signs of compromise. Thymic transcriptome analyses revealed a strong interferon response and downregulation of cell cycle and DNA repair pathways in VS and MS fetuses compared to CR and PR fetuses. Severe infection (MS) was further associated with downregulation of genes involved in early thymocyte development, suggesting disrupted T cell development in the thymus. Interaction expression quantitative trait loci (ieQTLs) were identified, where the association between genetic variants and expression levels of differentially expressed genes (DEGs) varied by fetal PRRS susceptibility. Notably, ieQTLs were identified for genes critical for T cell development, including TMEM98 (involved in Th1 cell differentiation) and PTCRA (expressed in early stages of thymocyte development). These findings highlight the complex interplay between fetal genotype, thymic gene expression, and PRRS susceptibility, offering potential genetic markers for breeding programs for replacement gilts.
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Registered trials
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