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需要 ESCRT 时:病毒装配位点的性质提示核病毒出核与逆转录病毒出芽之间存在机制相似性。

When in Need of an ESCRT: The Nature of Virus Assembly Sites Suggests Mechanistic Parallels between Nuclear Virus Egress and Retroviral Budding.

机构信息

Department of Molecular and Cell Biology, California Institute for Quantitative Biosciences, University of California-Berkeley, Berkeley, CA 94720, USA.

出版信息

Viruses. 2021 Jun 13;13(6):1138. doi: 10.3390/v13061138.

DOI:10.3390/v13061138
PMID:34199191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8231873/
Abstract

The proper assembly and dissemination of progeny virions is a fundamental step in virus replication. As a whole, viruses have evolved a myriad of strategies to exploit cellular compartments and mechanisms to ensure a successful round of infection. For enveloped viruses such as retroviruses and herpesviruses, acquisition and incorporation of cellular membrane is an essential process during the formation of infectious viral particles. To do this, these viruses have evolved to hijack the host Endosomal Sorting Complexes Required for Transport (ESCRT-I, -II, and -III) to coordinate the sculpting of cellular membrane at virus assembly and dissemination sites, in seemingly different, yet fundamentally similar ways. For instance, at the plasma membrane, ESCRT-I recruitment is essential for HIV-1 assembly and budding, while it is dispensable for the release of HSV-1. Further, HSV-1 was shown to recruit ESCRT-III for nuclear particle assembly and egress, a process not used by retroviruses during replication. Although the cooption of ESCRTs occurs in two separate subcellular compartments and at two distinct steps for these viral lifecycles, the role fulfilled by ESCRTs at these sites appears to be conserved. This review discusses recent findings that shed some light on the potential parallels between retroviral budding and nuclear egress and proposes a model where HSV-1 nuclear egress may occur through an ESCRT-dependent mechanism.

摘要

子代病毒粒子的正确组装和释放是病毒复制的基本步骤。总的来说,病毒已经进化出了无数种策略,利用细胞区室和机制来确保成功的感染循环。对于包膜病毒,如逆转录病毒和疱疹病毒,在形成感染性病毒颗粒的过程中,获取和整合细胞膜是一个必不可少的过程。为此,这些病毒进化出劫持宿主内体分选复合物必需运输(ESCRT-I、-II 和 -III)的能力,以协调病毒组装和释放部位的细胞膜塑形,以看似不同但在根本上相似的方式。例如,在质膜上,ESCRT-I 的募集对于 HIV-1 的组装和出芽是必不可少的,而对于 HSV-1 的释放则是可有可无的。此外,HSV-1 被证明募集 ESCRT-III 用于核粒子组装和出核,这是逆转录病毒在复制过程中不使用的过程。尽管 ESCRTs 的共表达发生在两个不同的细胞区室和两个不同的病毒生命周期步骤中,但 ESCRTs 在这些部位所起的作用似乎是保守的。这篇综述讨论了最近的发现,这些发现揭示了逆转录病毒出芽和核外逸之间可能存在的平行关系,并提出了一个模型,即 HSV-1 的核外逸可能通过一种依赖 ESCRT 的机制发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8567/8231873/22978e0c3a95/viruses-13-01138-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8567/8231873/3794b8725b6c/viruses-13-01138-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8567/8231873/62f6649401c2/viruses-13-01138-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8567/8231873/6abfaeb97fff/viruses-13-01138-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8567/8231873/22978e0c3a95/viruses-13-01138-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8567/8231873/3794b8725b6c/viruses-13-01138-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8567/8231873/62f6649401c2/viruses-13-01138-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8567/8231873/6abfaeb97fff/viruses-13-01138-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8567/8231873/22978e0c3a95/viruses-13-01138-g004.jpg

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