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致癌γ疱疹病毒的无效裂解复制对肿瘤微环境的调节作用。

Tumor Microenvironment Conditioning by Abortive Lytic Replication of Oncogenic γ-Herpesviruses.

机构信息

Viral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.

出版信息

Adv Exp Med Biol. 2020;1225:127-135. doi: 10.1007/978-3-030-35727-6_9.

DOI:10.1007/978-3-030-35727-6_9
PMID:32030652
Abstract

Epstein Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV) constitute the human γ-herpesviruses and two of the seven human tumor viruses. In addition to their viral oncogenes that primarily belong to the latent infection programs of these viruses, they encode proteins that condition the microenvironment. Many of these are early lytic gene products and are only expressed in a subset of infected cells of the tumor mass. In this chapter I will describe their function and the evidence that targeting them in addition to the latent oncogenes could be beneficial for the treatment of EBV- and KSHV-associated malignancies.

摘要

爱泼斯坦-巴尔病毒 (EBV) 和卡波西肉瘤相关疱疹病毒 (KSHV) 构成了人类 γ-疱疹病毒,也是七种人类肿瘤病毒中的两种。除了它们的病毒癌基因,这些癌基因主要属于这些病毒的潜伏感染程序外,它们还编码能够调节微环境的蛋白质。其中许多是早期裂解基因产物,仅在肿瘤块中受感染细胞的亚群中表达。在本章中,我将描述它们的功能以及针对这些病毒和潜伏癌基因的靶点进行治疗可能对 EBV 和 KSHV 相关恶性肿瘤有益的证据。

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本文引用的文献

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Plasmacytoid dendritic cells respond to Epstein-Barr virus infection with a distinct type I interferon subtype profile.浆细胞样树突状细胞对 Epstein-Barr 病毒感染的反应表现出独特的 I 型干扰素亚型谱。
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