Human enterovirus 71 subgenotype B3 lacks coxsackievirus A16-like neurovirulence in mice infection.
Human enterovirus 71 subgenotype B3 lacks coxsackievirus A16-like neurovirulence in mice infection.
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人类肠道病毒 71 亚基因型 B3 在小鼠感染中缺乏柯萨奇病毒 A16 样神经毒力。
DOI：
10.1186/1743-422x-2-74
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发表时间：
2005-08-26
期刊：
影响因子：
4.8
通讯作者：
AbuBakar S
中科院分区：
文献类型：
--
作者：
Chan YF;AbuBakar S
1998 年马来西亚爆发的一次疫情中至少鉴定出三种不同的 EV-71 亚基因型。亚基因型 C2 和 B4 与严重和致命感染相关，而 B3 病毒与轻度至亚临床感染相关。 B3病毒基因组序列与CV-A16的3'端相似性≥85%。这为检查 CV-A16、EV-71 B3 和 EV-71 B4 之间的毒力是否存在特征相似性和差异提供了机会，并确定 EV-71 B3 中 CV-A16 样基因的存在是否也会赋予该病毒在小鼠模型感染中具有 CV-A16 样神经毒力。对人肠道病毒71（EV-71）亚基因型B3基因组序列的分析表明，3D RNA聚合酶和3'非翻译区RNA二级结构的Z域与CV-A16具有高度相似性。与感染 EV-71 B4 的小鼠相比，一天大的小鼠脑内接种该病毒导致 16% 的小鼠出现后肢肿胀，并且体重增加显着降低。没有一只小鼠出现所有 CV-A16 感染小鼠中典型的后腿麻痹。从感染 CV-A16 的小鼠大脑中扩增出 CV-A16 基因组序列，但从所有接种 EV-71 的小鼠中未获得扩增，这表明乳鼠大脑中没有发生复制。这里提出的研究结果表明，EV-71 B3 病毒在基因组 3' 端具有类似 CV-A16 的非结构基因特征。它们的存在可能通过影响小鼠的总体健康来影响毒力，但不足以在小鼠模型感染中赋予 EV-71 B3 病毒类似 CV-A16 的神经毒力。
At least three different EV-71 subgenotypes were identified from an outbreak in Malaysia in 1998. The subgenotypes C2 and B4 were associated with the severe and fatal infections, whereas the B3 virus was associated with mild to subclinical infections. The B3 virus genome sequences had ≥85% similarity at the 3' end to CV-A16. This offers opportunities to examine if there are characteristic similarities and differences in virulence between CV-A16, EV-71 B3 and EV-71 B4 and to determine if the presence of the CV-A16-liked genes in EV-71 B3 would also confer the virus with a CV-A16-liked neurovirulence in mice model infection. Analysis of human enterovirus 71 (EV-71) subgenotype B3 genome sequences revealed that the 3D RNA polymerase and domain Z of the 3'-untranslating region RNA secondary structure had high similarity to CV-A16. Intracerebral inoculation of one-day old mice with the virus resulted in 16% of the mice showing swollen hind limbs and significantly lower weight gain in comparison to EV-71 B4-infected mice. None of the mice presented with hind leg paralysis typical in all the CV-A16 infected mice. CV-A16 genome sequences were amplified from the CV-A16-infected mice brain but no amplification was obtained from all the EV-71-inoculated mice suggesting that no replication had taken place in the suckling mice brain. The findings presented here suggest that EV-71 B3 viruses had CV-A16-liked non-structural gene features at the 3'-end of the genome. Their presence could have affected virulence by affecting the mice general health but was insufficient to confer the EV-71 B3 virus a CV-A16-liked neurovirulence in mice model infection.