Foreign Animal Disease Research Unit, USDA-ARS, Plum Island Animal Disease Center, Greenport, NY, USA; Department of Veterinary Population Medicine, University of Minnesota, St. Paul, MN, USA.
Foreign Animal Disease Research Unit, USDA-ARS, Plum Island Animal Disease Center, Greenport, NY, USA.
Virology. 2018 Mar;516:115-126. doi: 10.1016/j.virol.2018.01.008. Epub 2018 Jan 12.
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 编码区缺失与牛的毒力降低有关；然而，其机制尚不清楚。我们比较了牛的实验感染，使用了具有毒力的口蹄疫病毒 O1 Campos（O1Ca）和一个缺失 3A 区 87-106 位氨基酸的突变体衍生物（O1Ca∆3A）。出乎意料的是，两种病毒在鼻咽黏膜的原发性感染相似。然而，虽然 O1Ca 引起病毒血症和暴发性临床疾病，但 O1Ca∆3A 感染是亚临床和无病毒血症的。两组鼻咽组织中抗病毒细胞因子的表达没有差异，这表明 O1Ca∆3A 的衰减是由于在牛细胞中的复制效率降低所致，而不是宿主反应的差异。这些结果表明，尽管 FMDV 3A 缺失赋予了牛临床减毒表型，但该缺失并不能阻止亚临床感染。这些发现对口蹄疫病毒在野外爆发时出现明显宿主限制株的情况具有重要意义。
