HPV18/16 衣壳嵌合体中感染性病毒的产生研究。
Study of infectious virus production from HPV18/16 capsid chimeras.
机构信息
Department of Microbiology and Immunology H107, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
出版信息
Virology. 2010 Sep 30;405(2):289-99. doi: 10.1016/j.virol.2010.05.019. Epub 2010 Jul 3.
Using the HPV18 genome as the backbone, we exchanged the HPV18 L2 or L1 genes with those of HPV16. The intertypical exchange of HPV18 L1 with the HPV16 L1 produced genomes that efficiently replicated and produced infectious virus. Genomes containing an intertypical exchange of HPV18 L2 for the HPV16 L2 failed to produce infectious virus in multiple independently derived cell lines. Using chimeric constructs of individual capsid proteins, we identified a type-specific domain at the N-terminus of the HPV18L1 capsid protein, which interferes with its ability to cooperate with the HPV16 L2 protein to form infectious viral particles. Deletion of this domain allows for the cooperation of the HPV18 L1 protein and HPV16 L2 protein and production of infectious progeny. In addition, cooperation of this N-terminal HPV18 L1 deletion mutant protein with the wild-type HPV18 L2 protein efficiently replicates infectious virus but changes occur in the viral structure.
我们以 HPV18 基因组为骨架，将 HPV16 的 HPV18 L2 或 L1 基因与 HPV18 的 L2 或 L1 基因进行了交换。HPV18 L1 与 HPV16 L1 的异型交换产生了能够有效复制和产生感染性病毒的基因组。含有 HPV18 L2 与 HPV16 L2 异型交换的基因组在多个独立衍生的细胞系中均无法产生感染性病毒。使用单个衣壳蛋白的嵌合构建体，我们鉴定出 HPV18L1 衣壳蛋白 N 端的一个型特异性结构域，该结构域干扰了其与 HPV16 L2 蛋白形成感染性病毒颗粒的能力。该结构域的缺失允许 HPV18 L1 蛋白与 HPV16 L2 蛋白的合作，并产生感染性后代。此外，该 N 端 HPV18 L1 缺失突变蛋白与野生型 HPV18 L2 蛋白的合作能够有效地复制感染性病毒，但病毒结构会发生变化。
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