Tershak D R
J Virol. 1982 Feb;41(2):615-25. doi: 10.1128/JVI.41.2.615-625.1982.
A mixture containing standard poliovirus and D3 particles (mutants with deletions in the capsid locus) was serially passaged in the presence of guanidine. Within five growth cycles, the standard virus was guanidine resistant, but the D3 particles were guanidine sensitive, even after 21 passages with the inhibitor. By passage 40 with guanidine, D3 particles were eliminated, and a new deletion mutant (DX) appeared in the virus population. D3 particles contained a 15% deletion, and DX particles contained a 6% deletion in the capsid locus. Although neither mutant induced the synthesis of NCVP1a or a complete complement of capsid proteins after infection, cells infected with DX particles produced two novel proteins, which had molecular weights of approximately 68,000 and 25,000.
含有标准脊髓灰质炎病毒和D3颗粒（衣壳基因座有缺失的突变体）的混合物在胍存在的情况下连续传代。在五个生长周期内，标准病毒对胍具有抗性，但D3颗粒对胍敏感，即使在用该抑制剂传代21次后仍是如此。到用胍传代40次时，D3颗粒被消除，并且在病毒群体中出现了一种新的缺失突变体（DX）。D3颗粒在衣壳基因座中有15%的缺失，而DX颗粒在衣壳基因座中有6%的缺失。尽管这两种突变体在感染后均未诱导非衣壳病毒蛋白1a（NCVP1a）的合成或衣壳蛋白的完整互补，但用DX颗粒感染的细胞产生了两种新蛋白，其分子量约为68,000和25,000。
