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本文引用的文献

1
The evolving field of human papillomavirus receptor research: a review of binding and entry.人乳头瘤病毒受体研究的演进领域:结合和进入的综述。
J Virol. 2013 Jun;87(11):6062-72. doi: 10.1128/JVI.00330-13. Epub 2013 Mar 27.
2
Taking the gritty approach.采取坚定的方法。
IAVI Rep. 2012 Nov-Dec;16(4):4-7, 19.
3
Identification of a role for the trans-Golgi network in human papillomavirus 16 pseudovirus infection.鉴定跨高尔基网络在人乳头瘤病毒 16 假病毒感染中的作用。
J Virol. 2013 Apr;87(7):3862-70. doi: 10.1128/JVI.03222-12. Epub 2013 Jan 23.
4
Tetraspanin CD151 mediates papillomavirus type 16 endocytosis.四跨膜蛋白 CD151 介导人乳头瘤病毒 16 内吞作用。
J Virol. 2013 Mar;87(6):3435-46. doi: 10.1128/JVI.02906-12. Epub 2013 Jan 9.
5
Cellular entry of human papillomavirus type 16 involves activation of the phosphatidylinositol 3-kinase/Akt/mTOR pathway and inhibition of autophagy.人乳头瘤病毒 16 型的细胞进入涉及磷酸肌醇 3-激酶/Akt/mTOR 途径的激活和自噬的抑制。
J Virol. 2013 Mar;87(5):2508-17. doi: 10.1128/JVI.02319-12. Epub 2012 Dec 19.
6
Kinetic and HPV infection effects on cross-type neutralizing antibody and avidity responses induced by Cervarix(®).动力学和 HPV 感染对 Cervarix(®)诱导的交叉型中和抗体和亲和力反应的影响。
Vaccine. 2012 Dec 17;31(1):165-70. doi: 10.1016/j.vaccine.2012.10.067. Epub 2012 Oct 31.
7
SNX17 facilitates infection with diverse papillomavirus types.SNX17 有助于多种乳头瘤病毒类型的感染。
J Virol. 2013 Jan;87(2):1270-3. doi: 10.1128/JVI.01991-12. Epub 2012 Oct 31.
8
Use of an in vivo animal model for assessing the role of integrin α(6)β(4) and syndecan-1 in early steps in papillomavirus infection.利用体内动物模型评估整合素 α(6)β(4)和 syndecan-1 在 HPV 感染早期步骤中的作用。
Virology. 2012 Nov 25;433(2):395-400. doi: 10.1016/j.virol.2012.08.032. Epub 2012 Sep 18.
9
Host-cell factors involved in papillomavirus entry.参与乳头瘤病毒进入的宿主细胞因子。
Med Microbiol Immunol. 2012 Nov;201(4):437-48. doi: 10.1007/s00430-012-0270-1. Epub 2012 Sep 13.
10
Understanding and learning from the success of prophylactic human papillomavirus vaccines.理解和借鉴预防性人乳头瘤病毒疫苗的成功经验。
Nat Rev Microbiol. 2012 Oct;10(10):681-92. doi: 10.1038/nrmicro2872. Epub 2012 Sep 10.

乳头瘤病毒主要衣壳蛋白 L1。

The papillomavirus major capsid protein L1.

机构信息

Lab of Cellular Oncology, Center for Cancer Research, NCI, USA.

出版信息

Virology. 2013 Oct;445(1-2):169-74. doi: 10.1016/j.virol.2013.05.038. Epub 2013 Jun 22.

DOI:10.1016/j.virol.2013.05.038
PMID:23800545
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3783536/
Abstract

The elegant icosahedral surface of the papillomavirus virion is formed by a single protein called L1. Recombinant L1 proteins can spontaneously self-assemble into a highly immunogenic structure that closely mimics the natural surface of native papillomavirus virions. This has served as the basis for two highly successful vaccines against cancer-causing human papillomaviruses (HPVs). During the viral life cycle, the capsid must undergo a variety of conformational changes, allowing key functions including the encapsidation of the ~8 kb viral genomic DNA, maturation into a more stable state to survive transit between hosts, mediating attachment to new host cells, and finally releasing the viral DNA into the newly infected host cell. This brief review focuses on conserved sequence and structural features that underlie the functions of this remarkable protein.

摘要

乳头瘤病毒病毒粒子的优雅的二十面体表面由一种称为 L1 的单一蛋白质形成。重组 L1 蛋白可以自发地自我组装成一种高度免疫原性的结构,该结构与天然乳头瘤病毒病毒粒子的自然表面非常相似。这是针对致癌型人乳头瘤病毒 (HPV) 的两种非常成功的疫苗的基础。在病毒生命周期中,衣壳必须经历多种构象变化,从而允许包括以下关键功能:将约 8kb 的病毒基因组 DNA 包裹在内、成熟为更稳定的状态以在宿主之间的运输过程中存活、介导与新宿主细胞的附着,以及最终将病毒 DNA释放到新感染的宿主细胞中。本综述重点介绍了构成这种出色蛋白质功能基础的保守序列和结构特征。