Ability of foot-and-mouth disease virus to form plaques in cell culture is associated with suppression of alpha/beta interferon
Ability of foot-and-mouth disease virus to form plaques in cell culture is associated with suppression of alpha/beta interferon
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DOI：
10.1128/jvi.73.12.9891-9898.1999
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发表时间：
1999-12-01
影响因子：
5.4
通讯作者：
Grubman, MJ
中科院分区：
文献类型：
--
作者：
Chinsangaram, J;Piccone, ME;Grubman, MJ
缺乏前导蛋白酶编码区 (A12-LLV2) 的口蹄疫病毒遗传变体在牛和猪中均减毒，与野生型病毒 (A12-IC) 相比，牛气溶胶暴露后不会从初始感染部位传播。 A12-IC感染，不产生斑块；这一结果表明这种病毒不能从最初感染的部位传播到邻近的细胞。尽管如此，A12-LLV2 可以感染这些细胞，但与 A12-IC 感染相比，细胞病变效应和病毒产量显着降低。逆转录-PCR分析表明，A12-LLV2和A12-IC均诱导宿主细胞中α/β干扰素(IFN-α/β) mRNA的产生，然而，只有来自A12-LLV2感染细胞的上清液具有显着的抗病毒活性。 A12-LLV2 感染的胚胎牛肾细胞上清液中的抗病毒活性是 IFN-α/β 特异性的，用有或没有 IFN-α/β 受体的小鼠胚胎成纤维细胞进行测定。细胞培养物获得的结果表明，A12-IC 形成斑块的能力与 IFN-α/β 表达的抑制有关，并表明该宿主因子在 A12-LLV2 无法扩散和引起感染的过程中发挥了作用。易感动物的疾病。
A genetic variant of foot-and-mouth disease virus lacking the leader proteinase coding region (A12-LLV2) is attenuated in both cattle and swine and, in contrast to wild-type virus (A12-IC), does not spread from the initial site of infection after aerosol exposure of bovines, We have identified secondary cells from susceptible animals, i.e., bovine, ovine, and porcine animals, in which infection with A12-LLV2, in contrast to A12-IC infection, does not produce plaques; this result indicates that this virus cannot spread from the site of initial infection to neighboring cells. Nevertheless, A12-LLV2 can infect these cells, but cytopathic effects and virus yields are significantly reduced compared to those seen with A12-IC infection. Reverse transcription-PCR analysis demonstrates that both A12-LLV2 and A12-IC induce the production of alpha/beta interferon (IFN-alpha/beta) mRNA in host cells, However, only supernatants from A12-LLV2-infected cells have significant antiviral activity. The antiviral activity in supernatants from A12-LLV2-infected embryonic bovine kidney cells is IFN-alpha/beta specific, as assayed with mouse embryonic fibroblast cells with or without IFN-alpha/beta receptors, The results obtained with cell cultures demonstrate that the ability of A12-IC to form plaques is associated with the suppression of IFN-alpha/beta expression and suggest a role for this host factor in the inability of A12-LLV2 to spread and cause disease in susceptible animals.