Milken Institute School of Public Health Poster Presentations (Marvin Center & Video)

Title

Understanding fetal immune responses to congenital porcine reproductive and respiratory syndrome virus infection

Poster Number

65

Document Type

Poster

Status

Graduate Student - Masters

Abstract Category

Epidemiology and Biostatistics

Keywords

fetal infection; PRRSV; immunology

Publication Date

4-2017

Abstract

Porcine Reproductive and Respiratory Syndrome (PRRS) is one of the most economically significant diseases in the global swine industry, causing approximately $600 million annually in productivity losses in the United States alone. While this virus can cause a respiratory infection, it can also cross through the maternal endometrium and fetal placenta during late gestation and cause congenital infections and fetal death. Studying the extent to which the disease affects growing fetuses has been difficult because it is variable between gilts (a young female pig who has not had a litter) and between fetuses in her litter. Few studies have previously explored the immune pathways that alter fetal PRRS resistance/ susceptibility. We used a model where 3rd trimester pregnant gilts were euthanized at 2, 5, 8, 12, or 14 days post infection (DPI) with PRRS virus (PRRSV). Samples from the fetal thymus and placenta, and maternal endometrium were collected and viral loads measured (U Saskatchewan) to determine when the virus crosses the placental barrier and the level of PRRSV infection in each tissue. Fetal RNA was extracted with a Qiagen RNA Isolation kit, and gene expression was determined using a 230-gene swine immune NanoString array to evaluate differential expression (DE) of genes and biomarkers previously predicted to alter PRRS resistance and susceptibility. Biomarkers included measures of innate immunity, interferon signaling, B and T cell receptors, cell division, apoptosis, tissue remodeling and epithelial integrity, based on pathways identified using Ingenuity Pathway Analysis. Neighboring fetuses from PRRSV infected gilts from the same DPI but with different infection statuses and viral levels will be compared to determine DE genes between fetuses, litters and across DPI. Data should reveal immunological pathways that contribute to fetal susceptibility or resistance. Understanding these mechanisms will benefit future research dedicated to exploring targeted approaches to halt the congenital spread of this disease.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

Open Access

1

Comments

Poster to be presented at GW Annual Research Days 2017.

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Understanding fetal immune responses to congenital porcine reproductive and respiratory syndrome virus infection

Porcine Reproductive and Respiratory Syndrome (PRRS) is one of the most economically significant diseases in the global swine industry, causing approximately $600 million annually in productivity losses in the United States alone. While this virus can cause a respiratory infection, it can also cross through the maternal endometrium and fetal placenta during late gestation and cause congenital infections and fetal death. Studying the extent to which the disease affects growing fetuses has been difficult because it is variable between gilts (a young female pig who has not had a litter) and between fetuses in her litter. Few studies have previously explored the immune pathways that alter fetal PRRS resistance/ susceptibility. We used a model where 3rd trimester pregnant gilts were euthanized at 2, 5, 8, 12, or 14 days post infection (DPI) with PRRS virus (PRRSV). Samples from the fetal thymus and placenta, and maternal endometrium were collected and viral loads measured (U Saskatchewan) to determine when the virus crosses the placental barrier and the level of PRRSV infection in each tissue. Fetal RNA was extracted with a Qiagen RNA Isolation kit, and gene expression was determined using a 230-gene swine immune NanoString array to evaluate differential expression (DE) of genes and biomarkers previously predicted to alter PRRS resistance and susceptibility. Biomarkers included measures of innate immunity, interferon signaling, B and T cell receptors, cell division, apoptosis, tissue remodeling and epithelial integrity, based on pathways identified using Ingenuity Pathway Analysis. Neighboring fetuses from PRRSV infected gilts from the same DPI but with different infection statuses and viral levels will be compared to determine DE genes between fetuses, litters and across DPI. Data should reveal immunological pathways that contribute to fetal susceptibility or resistance. Understanding these mechanisms will benefit future research dedicated to exploring targeted approaches to halt the congenital spread of this disease.