Porcine reproductive and respiratory syndrome virus (PRRSV) preferentially infected the apical surface of primary endometrial cell monolayer
The underlying mechanism of porcine reproductive and respiratory syndrome virus (PRRSV) causing reproductive
failure and re-circulation in herds has remained unclear. Endometrial cells primarily infected with PRRSV may serve
as a significant target for PRRSV eradication. Primary endometrial (PE) cells from the porcine uterus were isolated and
cultivated to pursue this possibility. Immunocytochemistry analysis revealed the protein expression of classical
estrogen receptors (ER- and ER-), but not PRRSV receptors, CD163 and sialoadhesin in PE cells. PE cells were
apically/basolaterally inoculated with PRRSV type I/type II isolated from PRRSV infected lungs or mock infection.
Cytopathic effects (CPE) and PRRSV-GP5 positive cells were detected in PE cells incubated with PRRSV inoculum (107
TCID50/ml) beginning at 4 days post inoculation (dpi). Only apical inoculation produced effects, suggesting route
dependence of PRRSV infectivity in PE cells (p<0.05). PRRSV type II produced overall effects i.e., CPE, PRRSV-GP5
positive cells and a viral load higher than type I (p<0.05) during 2-6 dpi. In accordance with these effects, the tissue
epithelial resistance (TER) of type II inoculated PE cells was lower than that of mock or type I inoculated cells (p<0.05).
In addition, all the PE cells and media samples collected from PRRSV-inoculated PE cells persistently revealed PRRSVGP5 protein and viral copies (102-108 TCID50/ml) accessed by infecting MARC-145 cells. These findings provided the
first evidence that PE cells can be directly infected with PRRSV, favorably by type II at the apical side. However, all
PRRSV contaminated PE cells persistently carry the progeny virus.