Comprehensive pathogenesis studies on Peste des Petits Ruminants virus (PPRV) have been delayed so far by the absence of a small animal model reproducing the disease or an in vitro biological system revealing virulence differences. In this study, a mouse 10T1/2 cell line has been identified as presenting different susceptibility to virulent and attenuated PPRV strains. As evidenced by immunofluorescence test and RT-PCR, both virulent and attenuated PPR viruses penetrated and initiated the replication cycle in 10T1/2 cells, independently of the presence of the SLAM goat receptor. However, only virulent strains successfully completed their replication cycle while the vaccine strains did not. Since 10T1/2 cells are interferon-producing cells, the role of the type I interferon (type I IFN) response on this differentiated replication between virulent and attenuated strains was verified by stimulation or repression. Modulation of the type I IFN response did not improve the replication of the vaccine strains, indicating that other cell factor(s) not yet established may hinder the replication of attenuated PPRV in 10T1/2. This 10T1/2 cell line can be proposed as a new in vitro tool for PPRV-host interaction and virulence studies.

迄今为止，由于缺乏可复制该疾病的小型动物模型或体外方法，Peste des Petits反刍动物病毒（PPRV）的全面发病机理研究已被推迟揭示毒力差异的生物系统。在这项研究中，已确定小鼠​​10T1 / 2细胞系对强毒和减毒PPRV株表现出不同的敏感性。免疫荧光测试和RT-PCR证明，有毒和减毒的PPR病毒都可以穿透并启动10T1 / 2细胞中的复制周期，而与SLAM山羊受体的存在无关。但是，只有强毒株才能成功完成其复制周期，而疫苗株则没有。由于10T1 / 2细胞是产生干扰素的细胞，因此通过刺激或抑制可以验证I型干扰素（I型IFN）应答在有毒和减毒菌株之间这种差异复制中的作用。I型IFN反应的调节不能改善疫苗株的复制，表示尚未建立的其他细胞因子可能会阻碍减毒PPRV在10T1 / 2中的复制。该10T1 / 2细胞系可以作为新的PPRV-宿主相互作用和毒力研究的体外工具。