Deletions within the 3A coding region of foot-and-mouth disease virus (FMDV) are associated with decreased virulence in cattle; however, the mechanisms are unknown. We compared experimental infection of cattle with virulent FMDV O1Campos (O1Ca) and a mutant derivative (O1Ca∆3A) lacking residues 87–106 of 3A. Unexpectedly, primary infection of the nasopharyngeal mucosa was similar for both viruses. However, while O1Ca caused viremia and fulminant clinical disease, O1Ca∆3A infection was subclinical and aviremic. There were no differences in expression of anti-viral cytokines in nasopharyngeal tissues between the groups, suggesting attenuation by O1Ca∆3A was a consequence of reduced replication efficiency in bovine cells, rather than a difference in the host response. These results demonstrated that although deletion in 3A of FMDV confers a clinically attenuated phenotype in cattle, the deletion does not prevent subclinical infection. These findings have implications for field scenarios involving outbreaks with apparently host-limited strains of FMDV.

口蹄疫病毒（FMDV）3A编码区内的缺失与牛的毒力降低有关；但是，机制尚不清楚。我们比较了FMDV O1Campos（O1Ca）和缺乏3A残基87–106的突变体衍生物（O1Ca∆3A）对牛的实验性感染。出乎意料的是，两种病毒的鼻咽粘膜原发感染相似。然而，尽管O1Ca引起病毒血症和暴发性临床疾病，但O1Ca∆3A感染是亚临床性和非球蛋白血症。两组之间鼻咽组织中抗病毒细胞因子的表达没有差异，表明O1Ca∆3A的减弱是牛细胞复制效率降低的结果，而不是宿主反应的差异。这些结果表明，尽管FMDV 3A中的缺失赋予了牛临床上减毒的表型，但该缺失并不能预防亚临床感染。这些发现对野外场景具有明显的宿主有限的FMDV毒株暴发的影响。