Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA.
Virus Res. 2011 Sep;160(1-2):246-55. doi: 10.1016/j.virusres.2011.06.024. Epub 2011 Jul 6.
Papillomaviruses (PVs) comprise a large family of viruses infecting nearly all vertebrate species, with more than 100 human PVs identified. Our previous studies showed that a mutant chimera HPV18/16 genome, consisting of the upper regulatory region and early ORFs of HPV18 and the late ORFs of HPV16, was capable of producing infectious virus in organotypic raft cultures. We were interested in determining whether the ability of this chimeric genome to produce infectious virus was the result of HPV18 and HPV16 being similarly oncogenic, anogenital types and whether more disparate PV types could also interact functionally. To test this we created a series of HPV18 chimeric genomes where the ORFs for the HPV18 capsid genes were replaced with the capsid genes of HPV45, HPV39, HPV33, HPV31, HPV11, HPV6b, HPV1a, CRPV, and BPV1. All chimeras were able to produce infectious chimeric viral particles, although with lower infectivity than wild-type HPV18. Steps in the viral life cycle and characteristics of the viral particles were examined to identify potential causes for the decrease in infectivity.
乳头瘤病毒（PVs）是一类感染几乎所有脊椎动物物种的大型病毒家族，已鉴定出超过 100 种人类 PVs。我们之前的研究表明，一种由 HPV18 和 HPV16 的早期 ORFs 和晚期 ORFs 组成的 HPV18/16 突变嵌合基因组，能够在器官型筏培养物中产生感染性病毒。我们感兴趣的是确定这种嵌合基因组产生感染性病毒的能力是否是 HPV18 和 HPV16 具有相似致癌性、肛门生殖器类型的结果，以及是否更多不同的 PV 类型也可以进行功能交互。为了测试这一点，我们创建了一系列 HPV18 嵌合基因组，其中 HPV18 衣壳基因的 ORFs 被 HPV45、HPV39、HPV33、HPV31、HPV11、HPV6b、HPV1a、CRPV 和 BPV1 的衣壳基因取代。所有嵌合体都能够产生感染性嵌合病毒颗粒，尽管感染性比野生型 HPV18 低。检查了病毒生命周期的各个步骤和病毒颗粒的特征，以确定感染性降低的潜在原因。
