Coevolution of persistently infecting small DNA viruses and their hosts linked to host-interactive regulatory domains.
Coevolution of persistently infecting small DNA viruses and their hosts linked to host-interactive regulatory domains.
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持续感染的小 DNA 病毒及其宿主与宿主相互作用调控域的共同进化。
DOI：
10.1073/pnas.90.9.4117
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发表时间：
1993
影响因子：
11.1
通讯作者：
Villarreal,LP
中科院分区：
文献类型：
--
作者：
Shadan,FF;Villarreal,LP
虽然大多数RNA病毒基因组(和相关的细胞逆转录病毒)的进化速度可以比它们的宿主基因组快一百万倍，但一些小型DNA病毒(多瘤病毒和乳头瘤病毒)的进化速度似乎要慢得多。这些DNA病毒通常会引起宿主物种特有的隐匿性原发感染，然后是终生的良性持续性感染。通过对肾脏特异性多核病毒科(小鼠、仓鼠、灵长类、人类)进行全球序列比对，我们构建了病毒衣壳蛋白(VP1、VP2/VP3)和大肿瘤(T)抗原的简约进化树。我们表明，这三个编码序列可以产生彼此相似的系统发育树，以及与它们的宿主物种相似的系统发育树。这种病毒-宿主“共物种形成”似乎与一些流行的病毒进化观点不一致，我们认为，隐性持续感染可能将病毒和大多数宿主进化联系在一起。相似性分析发现，多瘤调节基因产物(T抗原)的三个特定区域高度保守，其中两个区域对应于宿主调节蛋白的结合位点(视网膜母细胞瘤基因产物p105和相关蛋白p107)。P53位点与保守的ATPase结构域重叠，视网膜母细胞瘤部位对应于5型腺病毒E1a蛋白的保守区域1。我们检测了这些结合序列的局部保守性，发现保守的视网膜母细胞瘤结合结构域是整个多瘤病毒家族的特征和包含，但保守的P53样结合结构域是特征的，并且包括三个完整的小DNA病毒家族：多瘤病毒、乳头瘤病毒和细小病毒。因此，小DNA病毒家族的进化可能通过与宿主调节蛋白的子集相互作用而与宿主进化和物种形成密切相关。
Although most RNA viral genomes (and related cellular retroposons) can evolve at rates a millionfold greater than that of their host genomes, some of the small DNA viruses (polyomaviruses and papillomaviruses) appear to evolve at much slower rates. These DNA viruses generally cause host species-specific inapparent primary infections followed by life-long, benign persistent infections. Using global progressive sequence alignments for kidney-specific Polyomaviridae (mouse, hamster, primate, human), we have constructed parsimonious evolutionary trees for the viral capsid proteins (VP1, VP2/VP3) and the large tumor (T) antigen. We show that these three coding sequences can yield phylogenetic trees similar to each other and to that of their host species. Such virus-host "co-speciation" appears incongruent with some prevailing views of viral evolution, and we suggest that inapparent persistent infections may link virus and most host evolution. Similarity analysis identified three specific regions of polyoma regulatory gene products (T antigens) as highly conserved, and two of these regions correspond to binding sites for host regulatory proteins (p53, the retinoblastoma gene product p105, and the related protein p107). The p53 site overlaps with a conserved ATPase domain and the retinoblastoma site corresponds to conserved region 1 of E1A protein of adenovirus type 5. We examined the local conservation of these binding sequences and show that the conserved retinoblastoma binding domain is characteristic and inclusive of the entire polyomavirus family, but the conserved p53-like binding domain is characteristic and inclusive of three entire families of small DNA viruses: polyomaviruses, papillomaviruses, and parvoviruses. The evolution of small-DNA-virus families may thus be tightly linked to host evolution and speciation by interaction with a subset of host regulatory proteins.