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疱疹病毒潜伏中的自噬逃逸。

Autophagy evasion in herpesviral latency.

机构信息

Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, CA, USA.

出版信息

Autophagy. 2010 Jan;6(1):151-2. doi: 10.4161/auto.6.1.10536. Epub 2010 Jan 4.

Abstract

Autophagy constitutes a major catabolic process for the quality control of internal proteins and organelles of eukaryotic cells, and is emerging as an essential part of the host antiviral defense. Many studies have shed light on the importance of autophagy in homeostasis, but it is not well understood how viruses co-opt the cellular autophagic pathway to establish virulence in vivo. Our recent study presents direct in vivo evidence for the key role of the anti-autophagic aspect of the virally encoded Bcl-2 proteins in the chronic infection of oncogenic gamma-herpesviruses and proposes that cellular autophagy may have a substantial effect on viral persistence and may influence the in vivo fitness of viruses. This discovery expands upon known antiviral activities of the autophagy machinery and also suggests new approaches for treating some virally induced diseases.

摘要

自噬是真核细胞内蛋白质和细胞器质量控制的主要分解代谢过程,它正在成为宿主抗病毒防御的重要组成部分。许多研究已经揭示了自噬在动态平衡中的重要性,但人们并不清楚病毒如何利用细胞自噬途径在体内建立毒力。我们最近的研究提供了直接的体内证据,证明病毒编码的 Bcl-2 蛋白的抗自噬方面在致癌性γ疱疹病毒的慢性感染中起着关键作用,并提出细胞自噬可能对病毒持续存在产生重大影响,并可能影响病毒在体内的适应性。这一发现扩展了自噬机制的已知抗病毒活性,也为治疗某些病毒诱导的疾病提供了新的方法。

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