Narechania Apurva, Chen Zigui, DeSalle Rob, Burk Robert D
Department of Microbiology, Albert Einstein College of Medicine, Ullman Building, Room 515, 1300 Morris Park Ave., Bronx, NY 10461, USA.
J Virol. 2005 Dec;79(24):15503-10. doi: 10.1128/JVI.79.24.15503-15510.2005.
The human papillomaviruses (HPVs) have long been thought to follow a monophyletic pattern of evolution with little if any evidence for recombination between genomes. On the basis of this model, both oncogenicity and tissue tropism appear to have evolved once. Still, no systematic statistical analyses have shown whether monophyly is the rule across all HPV open reading frames (ORFs). We conducted a taxonomic analysis of 59 mucosal/genital HPVs using whole-genome and sliding-window similarity measures; maximum-parsimony, neighbor-joining, and Bayesian phylogenetic analyses; and localized incongruence length difference (LILD) analyses. The algorithm for the LILD analyses localized incongruence by calculating the tree length differences between constrained and unconstrained nodes in a total-evidence tree across all HPV ORFs. The process allows statistical evaluation of every ORF/node pair in the total-evidence tree. The most significant incongruence was observed at the putative high-risk (i.e., cancer-associated) node, the common oncogenic ancestor for alpha HPV species 9 (e.g., HPV type 16 [HPV16]), 11, 7 (e.g., HPV18), 5, and 6. Although these groups share early-gene homology, including high degrees of similarity among E6 and E7, groups 9 and 11 diverge from groups 7, 5, and 6 with respect to L2 and L1. The HPV species groups primarily associated with cervical and anogenital cancers appear to follow two distinct evolutionary paths, one conferred by the early genes and another by the late genes. The incongruence in the genital HPV phylogeny could have occurred from an early recombination event, an ecological niche change, and/or asymmetric genome convergence driven by intense selection. These data indicate that the phylogeny of the oncogenic HPVs is complex and that their evolution may not be monophyletic across all genes.
长期以来,人们一直认为人乳头瘤病毒(HPV)遵循单系进化模式,几乎没有基因组间重组的证据。基于该模型,致癌性和组织嗜性似乎都只进化了一次。然而,尚无系统的统计分析表明单系性是否适用于所有HPV开放阅读框(ORF)。我们使用全基因组和滑动窗口相似性度量、最大简约法、邻接法和贝叶斯系统发育分析以及局部不一致长度差异(LILD)分析,对59种黏膜/生殖器HPV进行了分类学分析。LILD分析算法通过计算全证据树中所有HPV ORF的受约束节点和无约束节点之间的树长差异来定位不一致性。该过程允许对全证据树中的每个ORF/节点对进行统计评估。在假定的高危(即癌症相关)节点,即αHPV 9型(如HPV 16型[HPV16])、11型、7型(如HPV18型)、5型和6型的共同致癌祖先处,观察到最显著的不一致性。尽管这些组共享早期基因同源性,包括E6和E7之间的高度相似性,但9组和11组在L2和L1方面与7组、5组和6组不同。主要与宫颈癌和肛门生殖器癌相关的HPV物种组似乎遵循两条不同的进化路径,一条由早期基因赋予,另一条由晚期基因赋予。生殖器HPV系统发育中的不一致性可能源于早期重组事件、生态位变化和/或由强烈选择驱动的不对称基因组趋同。这些数据表明,致癌HPV的系统发育是复杂的,其进化在所有基因中可能不是单系的。