ArticlePloS one2017
Type 2 porcine reproductive and respiratory syndrome virus infection increases apoptosis at the maternal-fetal interface in late gestation pregnant gilts.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Investigating the functional capacity of porcine uterine natural killer cells during a porcine reproductive and respiratory syndrome virus infection of pregnant gilts.Veterinary research · 2025Article
- A Comprehensive Review on Porcine Reproductive and Respiratory Syndrome Virus with Emphasis on Immunity.Vaccines · 2024Review
- Evasion strategies of porcine reproductive and respiratory syndrome virus.Frontiers in microbiology · 2023Review
- Effect of porcine reproductive and respiratory syndrome virus 2 on angiogenesis and cell proliferation at the maternal-fetal interface.Veterinary pathology · 2022Article
- Phenotypic Characterization of a Virulent PRRSV-1 Isolate in a Reproductive Model With and Without Prior Heterologous Modified Live PRRSV-1 Vaccination.Frontiers in veterinary science · 2022Article
- Influence of PRRSV-1 vaccination and infection on mononuclear immune cells at the maternal-fetal interface.Frontiers in immunology · 2022Article
- Fetal hypoxia and apoptosis following maternal porcine reproductive and respiratory syndrome virus (PRRSV) infection.BMC veterinary research · 2021Article
- Samples sizes required to accurately quantify viral load and histologic lesion severity at the maternal-fetal interface of PRRSV-inoculated pregnant gilts.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2021Article
- Commercial PRRS Modified-Live Virus Vaccines.Vaccines · 2021Review
- Differential responses in placenta and fetal thymus at 12 days post infection elucidate mechanisms of viral level and fetal compromise following PRRSV2 infection.BMC genomics · 2020Article
- Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection.Virus research · 2020Review
- Article
- Signaling pathways involved in regulating apoptosis induction in host cells upon PRRSV infection.Virus genes · 2019Review
- Global miRNA, lncRNA, and mRNA Transcriptome Profiling of Endometrial Epithelial Cells Reveals Genes Related to Porcine Reproductive Failure Caused by Porcine Reproductive and Respiratory Syndrome Virus.Frontiers in immunology · 2019Article
- Perturbation of Thymocyte Development Underlies the PRRS Pandemic: A Testable Hypothesis.Frontiers in immunology · 2019Article
- Complete Genome Sequence of a Novel Subgenotype of Porcine Reproductive and Respiratory Syndrome Virus Strain JX/CH/2016, Isolated in Jiangxi, China.Genome announcements · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of fetal death associated with porcine reproductive and respiratory syndrome (PRRS) is hypothesized to be a consequence of PRRS virus-induced apoptosis at the maternal-fetal interface (MFI). The objectives of this study were to evaluate distribution and degree of apoptosis in the uterine and fetal placental tissues during the experimental type 2 PRRS virus (PRRSV) infection and determine associations between apoptosis at the MFI, PRRSV RNA concentration and antigen staining intensity, PRRSV-induced microscopic lesions, and fetal preservation status. A total of 114 naïve, high-health pregnant gilts were inoculated with type 2 PRRSV on gestation day 85±1 with euthanasia 21 days later; 19 sham-inoculated gilts served as controls. Two hundred and fifty samples of uterine tissue with fetal placenta were selected based on negative, low PRRSV RNA, and high PRRSV RNA concentration (0, < or > 2.7 log10 copies/mg, respectively). TUNEL assay was used to detect apoptosis in the endometrium and at the MFI. PRRSV RNA concentration and numbers of PRRSV immunopositive cells in uterine and placental tissue were positively associated with the severity of apoptosis in the endometrium and the MFI (P<0.001, P<0.05 and P<0.001, respectively). The number of TUNEL positive cells at the MFI was also positively associated with the severity (P<0.001) of vasculitis, but not total numbers of inflammatory cells in the endometrium. Increased numbers of TUNEL positive cells at the MFI were associated with PRRSV load in the fetal thymus, and greater odds of meconium staining of the fetus at 21 days post infection (P<0.001 for both). These findings suggest an important role of apoptosis in the pathogenesis of uterine epithelial and trophoblastic cell death at the MFI. Moreover, apoptosis at the MFI is significantly associated with fetal demise during in utero type 2 PRRSV infection.
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