Three viruses of the bovine respiratory disease complex apply different strategies to initiate infection
Three viruses of the bovine respiratory disease complex apply different strategies to initiate infection
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DOI：
10.1186/1297-9716-45-20
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发表时间：
2014-02-18
影响因子：
4.4
通讯作者：
Herrler, Georg
中科院分区：
文献类型：
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作者：
Kirchhoff, Jana;Uhlenbruck, Sabine;Herrler, Georg
牛呼吸道疾病复合体(BRDC)是引起犊牛严重呼吸道感染的主要原因。这种疾病是多因素的，要么是压力，要么是免疫力下降，导致几种病原体出现。我们研究了牛呼吸道上皮细胞(BAEC)对与BRDC相关的三种主要病毒：牛呼吸道合胞病毒(BRSV)、牛疱疹病毒1型(BHV-1)和牛副流感病毒3型(BPIV3)感染的敏感性。为此，使用了两种分化良好的BAEC的培养系统：气液界面(ALI)系统和精密切割肺切片(PCLS)系统，在ALI系统中，滤器生长的BAEC分化为假复层呼吸道上皮；在PCLS系统中，BAEC保持在原始组织中。比较感染研究表明，BPIV3的进入和释放是通过根尖膜发生的，纤毛细胞是主要的靶细胞。相比之下，呼吸道上皮细胞在很大程度上对BHV-1感染具有抵抗力。当通过开放紧密连接或损伤细胞单层来消除上皮屏障时，BHV-1主要感染基底细胞。呼吸道上皮细胞对BRSV感染也有抵抗力。然而，当上皮屏障的完整性被破坏时，这种病毒既不感染分化的上皮细胞，也不感染基底细胞。与呼吸道上皮细胞相比，上皮下细胞易受BRSV感染。总之，这些结果表明，同一疾病复合体的三种病毒遵循不同的策略与呼吸道上皮相互作用。讨论了可能的进入机制。
Bovine respiratory disease complex (BRDC) is the major cause of serious respiratory tract infections in calves. The disease is multifactorial, with either stress or reduced immunity allowing several pathogens to emerge. We investigated the susceptibility of bovine airway epithelial cells (BAEC) to infection by the three major viruses associated with the BRDC: bovine respiratory syncytial virus (BRSV), bovine herpesvirus type 1 (BHV-1) and bovine parainfluenza virus type 3 (BPIV3). For this purpose, two culture systems for well-differentiated BAEC were used: the air-liquid interface (ALI) system, where filter-grown BAEC differentiate into a pseudostratified respiratory epithelium and precision-cut lung slices (PCLS) where BAEC are maintained in the original tissue organisation. Comparative infection studies demonstrated that entry and release of BPIV3 occurred specifically via the apical membrane with ciliated cells being the major target cells. By contrast, airway epithelial cells were largely resistant to infection by BHV-1. When the epithelial barrier was abolished by opening tight junctions or by injuring the cell monolayer, BHV-1 infected mainly basal cells. Respiratory epithelial cells were also refractory to infection by BRSV. However, this virus infected neither differentiated epithelial cells nor basal cells when the integrity of the epithelial barrier was destroyed. In contrast to cells of the airway epithelium, subepithelial cells were susceptible to infection by BRSV. Altogether, these results indicate that the three viruses of the same disease complex follow different strategies to interact with the airway epithelium. Possible entry mechanisms are discussed.