脊髓灰质炎减毒活疫苗（Sabin 3型）减毒的遗传基础
Genetic basis of attenuation of the Sabin type 3 oral poliovirus vaccine.
作者信息
Westrop G D, Wareham K A, Evans D M, Dunn G, Minor P D, Magrath D I, Taffs F, Marsden S, Skinner M A, Schild G C
机构信息
Department of Microbiology, University of Reading, United Kingdom.
出版信息
J Virol. 1989 Mar;63(3):1338-44. doi: 10.1128/JVI.63.3.1338-1344.1989.
Abstract
The poliovirus type 3 Sabin oral poliovirus vaccine strain P3/Leon/12a1b differs in nucleotide sequence from its neurovirulent progenitor P3/Leon/37 by just 10 point mutations. The contribution of each mutation to the attenuation phenotype of the vaccine strain was determined by the construction of a series of recombinant viruses from infectious cDNA clones. The neurovirulence testing of recombinant viruses indicated that the attenuation phenotype is determined by just two point mutations: a C to U in the noncoding region at position 472 and a C to U at nucleotide 2034 which results in a serine-to-phenylalanine amino acid substitution in the structural protein VP3.
摘要
脊髓灰质炎病毒3型萨宾口服脊髓灰质炎疫苗株P3/Leon/12a1b与其神经毒力祖代株P3/Leon/37的核苷酸序列仅相差10个点突变。通过从感染性cDNA克隆构建一系列重组病毒，确定了每个突变对疫苗株减毒表型的贡献。重组病毒的神经毒力测试表明，减毒表型仅由两个点突变决定：472位非编码区的C突变为U，以及2034位核苷酸的C突变为U，后者导致结构蛋白VP3中的丝氨酸到苯丙氨酸的氨基酸替换。
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