Ward R L, Knowlton D R, Greenberg H B
Division of Clinical Virology, James N. Gamble Institute of Medical Research, Cincinnati, Ohio 45219.
J Virol. 1988 Nov;62(11):4358-61. doi: 10.1128/JVI.62.11.4358-4361.1988.
Coinfection of MA-104 cells with serotype 1 (Wa strain) and serotype 3 (P strain) human rotaviruses resulted in progeny viruses that were phenotypically mixed in their major outer-shell structural-protein VP7 and in the genome segment that encodes this protein (segment 9). Segments from the Wa virus predominated in these progeny whether they were of parental or reassortant genotype. Neutralization with monoclonal antibodies specific for VP7 proteins of the coinfecting viruses caused an alteration in genomic distribution favoring the strain heterologous to the neutralizing monoclonal antibody. Because the percentage of change in distribution of segment 9 was similar to that of the other combined segments, there appeared to be no greater association between VP7 and segment 9 than with other segments of the homologous virus during encapsulation. From these results, it was calculated that the progeny of coinfection with P segment 9 were 77.4% mosaic structures and 14.8% pseudotypes; progeny of coinfection with Wa segment 9 were 40.2% mosaic structures and 1.3% pseudotypes. Similar determinations were made for the reassortant progeny alone.
MA - 104细胞被1型（Wa株）和3型（P株）人轮状病毒共感染后，产生的子代病毒在其主要外壳结构蛋白VP7以及编码该蛋白的基因组片段（片段9）上表现出表型混合。无论子代病毒是亲本基因型还是重配基因型，Wa病毒的片段在其中都占主导地位。用针对共感染病毒VP7蛋白的单克隆抗体进行中和作用，会导致基因组分布发生改变，有利于与中和性单克隆抗体异源的毒株。由于片段9分布的变化百分比与其他组合片段的相似，因此在病毒包装过程中，VP7与片段9之间的关联似乎并不比与同源病毒的其他片段更强。根据这些结果计算得出，感染P片段9产生的子代中有77.4%是嵌合结构，14.8%是假型；感染Wa片段9产生的子代中有40.2%是嵌合结构，1.3%是假型。对单独的重配子代也进行了类似的测定。
