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首页> 外文OA文献 >Cooperative Effect of the Attenuation Determinants Derived from Poliovirus Sabin 1 Strain Is Essential for Attenuation of Enterovirus 71 in the NOD/SCID Mouse Infection Model▿
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Cooperative Effect of the Attenuation Determinants Derived from Poliovirus Sabin 1 Strain Is Essential for Attenuation of Enterovirus 71 in the NOD/SCID Mouse Infection Model▿

机译：脊髓灰质炎沙宾1株减毒决定簇的协同效应对NOD / SCID小鼠感染模型中肠病毒71减毒至关重要。

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Enterovirus 71 (EV71) is a causative agent of hand, foot, and mouth disease and is also associated with serious neurological disorders. An attenuated EV71 strain [EV71(S1-3′)] has been established in the cynomolgus monkey infection model; this strain contains the attenuation determinants derived from the type 1 poliovirus vaccine strain, Sabin 1 [PV1(Sabin)], in the 5′ nontranslated region (NTR), 3D polymerase, and 3′ NTR. In this study, we analyzed the effect of the attenuation determinants of PV1(Sabin) on EV71 infection in a NOD/SCID mouse infection model. We isolated a mouse-adapted EV71 strain [EV71(NOD/SCID)] that causes paralysis of the hind limbs in 3- to 4-week-old NOD/SCID mice by adaptation of the virulent EV71(Nagoya) strain in the brains of NOD/SCID mice. A single mutation at nucleotide 2876 that caused an amino acid change in capsid protein VP1 (change of the glycine at position 145 to glutamic acid) was essential for the mouse-adapted phenotype in NOD/SCID mice. Next, we introduced attenuation determinants derived from PV1(Sabin) along with the mouse adaptation mutation into the EV71(Nagoya) genome. In 4-week-old mice, the determinants in the 3D polymerase and 3′ NTR, which are the major temperature-sensitive determinants, had a strong effect on attenuation. In contrast, the effect of individual determinants was weak in 3-week-old NOD/SCID mice, and all the determinants were required for substantial attenuation. These results suggest that a cooperative effect of the attenuation determinants of PV1(Sabin) is essential for attenuated neurovirulence of EV71.
机译：肠病毒71（EV71）是手足口病的病原体，也与严重的神经系统疾病有关。在食蟹猴感染模型中已经建立了减毒的EV71毒株[EV71（S1-3'）]；该菌株在5'非翻译区（NTR），3D聚合酶和3'NTR中包含源自1型脊髓灰质炎病毒疫苗株Sabin 1 [PV1（Sabin）]的减毒决定簇。在这项研究中，我们分析了在NOD / SCID小鼠感染模型中PV1（Sabin）衰减决定簇对EV71感染的影响。我们分离出了适应小鼠的EV71株[EV71（NOD / SCID）]，该株通过适应有毒的EV71（Nagoya）株在大脑中引起3至4周龄的NOD / SCID小鼠后肢瘫痪NOD / SCID小鼠。核苷酸2876处的单个突变会导致衣壳蛋白VP1的氨基酸发生变化（位置145处的甘氨酸变为谷氨酸），这对于NOD / SCID小鼠的小鼠适应表型至关重要。接下来，我们将源自PV1（Sabin）的衰减决定簇以及小鼠适应突变引入到EV71（Nagoya）基因组中。在4周龄的小鼠中，主要的温度敏感性决定因素3D聚合酶和3'NTR中的决定因素对减毒作用很大。相反，在3周龄的N​​OD / SCID小鼠中，各个决定因素的作用较弱，并且所有决定因素都需要进行实质性衰减。这些结果表明，PV1（Sabin）减毒决定簇的协同作用对于EV71的减毒神经毒力至关重要。

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