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小型 DNA 肿瘤病毒持续存在的机制。

Mechanisms of persistence by small DNA tumor viruses.

机构信息

Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

出版信息

Curr Opin Virol. 2018 Oct;32:71-79. doi: 10.1016/j.coviro.2018.09.002. Epub 2018 Oct 1.

Abstract

Virus infection contributes to nearly 15% of human cancers worldwide. Many of the oncogenic viruses tend to cause cancer in immunosuppressed individuals, but maintain asymptomatic, persistent infection for decades in the general population. In this review, we discuss the tactics employed by two small DNA tumor viruses, Human papillomavirus (HPV) and Merkel cell polyomavirus (MCPyV), to establish persistent infection. We will also highlight recent key findings as well as outstanding questions regarding the mechanisms by which HPV and MCPyV evade host immune control to promote their survival. Since persistent infection enables virus-induced tumorigenesis, identifying the mechanisms by which small DNA tumor viruses achieve latent infection may inform new approaches for preventing and treating their respective human cancers.

摘要

病毒感染导致了全球近 15%的人类癌症。许多致癌病毒往往会导致免疫抑制个体患上癌症,但在普通人群中,它们会保持数十年的无症状、持续性感染。在这篇综述中,我们讨论了两种小型 DNA 肿瘤病毒,人乳头瘤病毒 (HPV) 和 Merkel 细胞多瘤病毒 (MCPyV),它们用来建立持续性感染的策略。我们还将强调最近的关键发现,以及关于 HPV 和 MCPyV 逃避宿主免疫控制以促进其存活的机制的悬而未决的问题。由于持续性感染使病毒诱导的肿瘤发生成为可能,因此确定小型 DNA 肿瘤病毒实现潜伏感染的机制可能为预防和治疗其各自的人类癌症提供新的方法。

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