Relationship between vasculitis, endometrial inflammation and cell death at maternal-fetal interface of type 2 PRRSV infected pregnant gilts

Porcine reproductive and respiratory syndrome virus (PRRSV) is a well-known cause of reproductive failure worldwide. It is known that PRRSV can induce apoptosis under in-vitro conditions, and is significantly associated with cell the occurrence of cell death in multiple infected tissues invivo. The mechanism of cell death occurring at the maternal-fetal interface during PRRSV infection, and the relationship of cell death to the cytopathic effect of the PRRSV and other pathogenic factors remain unclear.

The objective of this study was to determine if the PRRSV induced endometrial inflammation and vasculitis along with presence of virus are associated with the occurrence of cell death at the maternal-fetal interface

A total of 114 PRRSV-naïve high-health pregnant gilts were inoculated with a type 2 PRRSV (NVSL 97-7895) and 19 negative control gilts were sham inoculated on gestation day 85±1. At 21days post inoculation (DPI), dams and their litters were humanely euthanized for necropsy examination. The adjacent uterus and placenta was graded based on the percentage of affected endometrial tissue and the total number of inflammatory cells present. The degree of vasculitis was assessed based on its distribution and severity within the endometrium. The same tissues (n=248) were also examined by TUNEL assay to detect apoptosis. Numbers of apoptotic cells per 1mm² area of the endometrium and fetal placenta were determined by Image ProPlus software.

Moderate lymphohistiocytic endometritis was in 60.48% (150/248) of the tissue sections. Grade 1 vasculitis was most common in 52.82% (131/248) of endometrial vasculature. However, statistical analysis revealed that only distribution and severity of vasculitis in combination with viral load have a significant positive association with the numbers of TUNEL positive cells at the maternal-fetal interface (P< 0.05, P< 0.001, P< 0.001, respectively; linear mixed model, clustering by gilt). Apoptosis was not significantly associated with the severity of inflammation affecting lamina propria, uterine gland and interdigitation areas of maternal-fetal interface.

In the related work from this project, there was no relationship found between the viral loads and the amount of endometrial inflammation within the uterus.

While the inflammation score was not associated with apoptosis, the findings from this project demonstrate a connection between vascular lesions in the pathogenesis of cell death at the maternal-fetal interface during type 2 PRRSV infection of pregnant gilts at 21 DPI. Further work examining this relationship at earlier time points in the infection process are underway.

Disclosure of Interest: None Declared.