Generation and characterization of a porcine endometrial endothelial cell line susceptible to porcine reproductive and respiratory syndrome virus

Relationships of CD163 and CD169 positive cell numbers in the endometrium and fetal placenta with type 2 PRRSV RNA concentration in fetal thymus

“…Nevertheless, it has been confirmed that some epithelial cells such as St-Jude porcine lung cells are susceptible to in vitro PRRSV infection due to the expression of receptor CD151 [ 39 ]. CD151 receptor has been also implicated in PRRSV infection of porcine endometrial endothelial cells, where it is believed to act as alternative receptor along with CD169 [ 40 ]. Additionally, syndecan-4, which is heparan sulfate proteoglycan, is confirmed to be required in the PRRSV attachment to MARC-145 cells [ 41 ].…”

Susceptibility of porcine pulmonary microvascular endothelial cells to porcine reproductive and respiratory syndrome virus

“…Although the endothelial cells from several tissues were demonstrated to be susceptible to PRRSV [4,18], some contrary results have been published by other researchers. For example, five strains of PRRSV were experimentally proven not capable of replication in cultures using large-vessel endothelial cells isolated from the aorta and pulmonary artery [6], from which the authors addressed the importance of undertaking further investigation with fetal and microvasculature-derived endothelium and other PRRSV strains.…”

“…Heparin sulfate, CD169 (sialoadhesin), CD163 (scavenger receptor), CD151, and vimentin have been identified as important receptors of PRRSV that perform diverse functions in different stages of viral infection [ 16 ] and are the main targets of investigation in alveolar macrophages or MARC-145 cells. Heparin sulfate and vimentin have been reported to be expressed on various endothelial cells [ 3 , 4 , 7 ], and the distributions of the remaining three receptor molecules in different cells are highly discrepant. Therefore, CD151, CD163, and CD169 were detected in this study.…”

“…Feng et al. [ 4 ] also found that CD151 and CD169, rather than CD163 were expressed in porcine endometrial endothelial cells, which displayed a high susceptibility to PRRSV. We speculate that the mechanism of infection of PRRSV in endothelial cells is different from that in alveolar macrophages or MARC-145 cells, and that the roles of CD151, heparin sulfate, and vimentin on PRRSV infection in PMECs warrant further investigation.…”

“…As evidenced by classical symptoms such as skin cyanosis [13], interstitial pneumonia [19], and viral antigen distribution in the endothelium [9] of PRRSV-infected piglets, endothelial injury and dysfunction should be involved in its pathogenesis, which has been highlighted in some literature. For example, porcine endothelial cells in the endometrium and carotid artery had been demonstrated to have a high susceptibility to PRRSV [4,18]. PRRSV infection could lead to severe endothelial dysfunction due to unbalanced expression of regulatory proteins, HSP90 and caveolin-1 [23], over-expression of inflammatory cytokines in vascular endothelial cells [8], and impairment of edema resolution by down-regulating the expression of aquaporin 1 and 5 in endothelial cells and secretory cells of terminal bronchiole [24].…”