Monocytes are considered refractory to porcine reproductive and respiratory syndrome virus type 1 (PRRSV-1) infection. However, monocytes are only short-lived in blood, being able to differentiate into macrophages and dendritic cells (DC). It was therefore merited to revisit PRRSV-1 interaction with monocytes, particularly those treated with cytokines influencing monocyte biology. Thus, several factors were screened, particularly those modulating monocyte differentiation and expression of putative PRRSV-1 receptors (CD169 and CD163). M-CSF, known to stimulate macrophage differentiation, did not increase their susceptibility to PRRSV-1. Nor did GM-CSF or IL-4, known drivers for monocyte-derived DC (MoDC) differentiation. In contrast, monocyte treatment with IL-10 or the corticosteroid, dexamethasone, known to be potent suppressors of monocyte differentiation, was correlated with increased susceptibility to PRRSV-1 infection. While this effect was strongly correlated to CD163 and CD169 expression, our data suggest that receptor expression is not the only factor driving successful infection of PPRSV-1 in monocytes.

单核细胞被认为对猪的生殖和呼吸综合征病毒1型（PRRSV-1）感染具有抵抗力。然而，单核细胞仅在血液中短暂存在，能够分化为巨噬细胞和树突状细胞（DC）。因此，值得回顾一下PRRSV-1与单核细胞的相互作用，特别是那些用影响单核细胞生物学的细胞因子治疗的单核细胞。因此，筛选了几个因素，特别是那些调节单核细胞分化和假定的PRRSV-1受体（CD169和CD163）表达的因素。已知可刺激巨噬细胞分化的M-CSF并未增加其对PRRSV-1的敏感性。GM-CSF或IL-4（单核细胞衍生的DC（MoDC）分化的已知驱动器）也没有。相比之下，用IL-10或皮质类固醇地塞米松治疗单核细胞，已知是单核细胞分化的有效抑制剂，与PRRSV-1感染的易感性增加相关。尽管此效应与CD163和CD169表达密切相关，但我们的数据表明受体表达并不是驱动单核细胞成功感染PPRSV-1的唯一因素。