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潜伏性卡波西肉瘤疱疹病毒感染期间细胞代谢的激活

Activation of cellular metabolism during latent Kaposi's Sarcoma herpesvirus infection.

作者信息

Lagunoff Michael

机构信息

Department of Microbiology, University of Washington, 1959 N.E. Pacific St., Box 347252, Seattle, WA 98195, United States.

出版信息

Curr Opin Virol. 2016 Aug;19:45-9. doi: 10.1016/j.coviro.2016.06.012. Epub 2016 Jul 18.

Abstract

Herpesviruses can establish latent infections in the host with severely limited viral gene expression. Kaposi's Sarcoma-associated herpesvirus (KSHV) is found predominantly in the latent state in the main KS tumor cell, a cell of endothelial origin. While many viruses alter host cell metabolism during productive infection, latent KSHV infection of endothelial cells activates metabolic pathways that are activated in many cancer cells. Inhibition of these major metabolic pathways leads to apoptotic cell death of the latently infected cells. The study of KSHV activation of metabolism may lead to novel therapeutic options for eliminating latent infection of gamma-herpesviruses and could also lead to a deeper mechanistic understanding of how to target cancer cell metabolism.

摘要

疱疹病毒能够在宿主中建立潜伏感染,此时病毒基因表达严重受限。卡波西肉瘤相关疱疹病毒(KSHV)主要以潜伏状态存在于卡波西肉瘤主要肿瘤细胞中,该细胞起源于内皮细胞。虽然许多病毒在增殖性感染期间会改变宿主细胞代谢,但内皮细胞的KSHV潜伏感染会激活许多癌细胞中被激活的代谢途径。抑制这些主要代谢途径会导致潜伏感染细胞发生凋亡性细胞死亡。对KSHV代谢激活的研究可能会带来消除γ-疱疹病毒潜伏感染的新治疗选择,也可能会更深入地从机制上理解如何靶向癌细胞代谢。

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