一种脊髓灰质炎病毒神经毒力的小鼠模型鉴定出了使该病毒对人类减毒的突变。
A mouse model for poliovirus neurovirulence identifies mutations that attenuate the virus for humans.
作者信息
La Monica N, Almond J W, Racaniello V R
出版信息
J Virol. 1987 Sep;61(9):2917-20. doi: 10.1128/JVI.61.9.2917-2920.1987.
Abstract
A mutation in the genome of poliovirus type 3 that is known to reduce neurovirulence in humans similarly reduces neurovirulence in mice when incorporated into a mouse-adapted-human poliovirus recombinant. Viral recombinants with a uracil at nucleotide position 472 in the 5'-noncoding regions of their genomes are unable to replicate in the mouse brain. Viral recombinants with a cytosine at this position are neurovirulent in mice. Neurovirulence of poliovirus in mice may therefore prove to be a useful indicator of the genetic stability of new attenuating mutations created by site-directed mutagenesis.
摘要
已知3型脊髓灰质炎病毒基因组中的一种突变可降低其对人类的神经毒性，当将该突变整合到适应小鼠的人脊髓灰质炎病毒重组体中时，同样会降低其对小鼠的神经毒性。基因组5'-非编码区核苷酸位置472处为尿嘧啶的病毒重组体无法在小鼠脑中复制。该位置为胞嘧啶的病毒重组体在小鼠中具有神经毒性。因此，脊髓灰质炎病毒在小鼠中的神经毒性可能被证明是通过定点诱变产生的新减毒突变遗传稳定性的有用指标。
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