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Anticipating the Next Ten Years of the Annual Review of Virology. 展望病毒学年度评论的未来十年。
IF 11.3 1区 医学 Q1 VIROLOGY Pub Date : 2023-09-29 DOI: 10.1146/annurev-vi-10-062723-101111
Julie K Pfeiffer, Lynn W Enquist, Daniel DiMaio, Terence S Dermody
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引用次数: 0
Structural and Functional Insights into Viral Programmed Ribosomal Frameshifting. 病毒程序性核糖体移框的结构和功能见解。
IF 11.3 1区 医学 Q1 VIROLOGY Pub Date : 2023-09-29 Epub Date: 2023-06-20 DOI: 10.1146/annurev-virology-111821-120646
Chris H Hill, Ian Brierley

Protein synthesis by the ribosome is the final stage of biological information transfer and represents an irreversible commitment to gene expression. Accurate translation of messenger RNA is therefore essential to all life, and spontaneous errors by the translational machinery are highly infrequent (∼1/100,000 codons). Programmed -1 ribosomal frameshifting (-1PRF) is a mechanism in which the elongating ribosome is induced at high frequency to slip backward by one nucleotide at a defined position and to continue translation in the new reading frame. This is exploited as a translational regulation strategy by hundreds of RNA viruses, which rely on -1PRF during genome translation to control the stoichiometry of viral proteins. While early investigations of -1PRF focused on virological and biochemical aspects, the application of X-ray crystallography and cryo-electron microscopy (cryo-EM), and the advent of deep sequencing and single-molecule approaches have revealed unexpected structural diversity and mechanistic complexity. Molecular players from several model systems have now been characterized in detail, both in isolation and, more recently, in the context of the elongating ribosome. Here we provide a summary of recent advances and discuss to what extent a general model for -1PRF remains a useful way of thinking.

核糖体合成蛋白质是生物信息传递的最后阶段,代表着对基因表达的不可逆转的承诺。因此,信使RNA的准确翻译对所有生命都至关重要,翻译机制的自发错误极为罕见(~1/100000密码子)。程序性-1核糖体移码(-1PRF)是一种机制,在这种机制中,伸长的核糖体被诱导在特定位置向后滑动一个核苷酸,并在新的阅读框中继续翻译。这被数百种RNA病毒用作翻译调控策略,它们在基因组翻译过程中依赖-1PRF来控制病毒蛋白质的化学计量。虽然1PRF的早期研究集中在病毒学和生物化学方面,但X射线晶体学和冷冻电镜(cryo-EM)的应用,以及深度测序和单分子方法的出现,揭示了意想不到的结构多样性和机制复杂性。来自几个模型系统的分子参与者现在已经得到了详细的表征,无论是在孤立的情况下,还是最近在延长核糖体的背景下。在这里,我们对最近的进展进行了总结,并讨论了-1PRF的通用模型在多大程度上仍然是一种有用的思维方式。
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引用次数: 0
Segmented, Negative-Sense RNA Viruses of Humans: Genetic Systems and Experimental Uses of Reporter Strains. 人类的分段负义RNA病毒:报告菌株的遗传系统和实验用途。
IF 8.1 1区 医学 Q1 VIROLOGY Pub Date : 2023-09-29 DOI: 10.1146/annurev-virology-111821-120445
Cait E Hamele, M Ariel Spurrier, Rebecca A Leonard, Nicholas S Heaton

Negative-stranded RNA viruses are a large group of viruses that encode their genomes in RNA across multiple segments in an orientation antisense to messenger RNA. Their members infect broad ranges of hosts, and there are a number of notable human pathogens. Here, we examine the development of reverse genetic systems as applied to these virus families, emphasizing conserved approaches illustrated by some of the prominent members that cause significant human disease. We also describe the utility of their genetic systems in the development of reporter strains of the viruses and some biological insights made possible by their use. To conclude the review, we highlight some possible future uses of reporter viruses that not only will increase our basic understanding of how these viruses replicate and cause disease but also could inform the development of new approaches to therapeutically intervene.

负链RNA病毒是一大类病毒,它们以信使RNA反义的方向将基因组编码在多个片段的RNA中。它们的成员感染广泛的宿主,还有许多值得注意的人类病原体。在这里,我们研究了应用于这些病毒家族的反向遗传系统的发展,强调了一些导致重大人类疾病的重要成员所展示的保守方法。我们还描述了它们的遗传系统在病毒报告株开发中的作用,以及它们的使用可能带来的一些生物学见解。为了总结这篇综述,我们强调了报告病毒未来可能的一些用途,这些用途不仅将增加我们对这些病毒如何复制和致病的基本了解,还可以为开发新的治疗干预方法提供信息。
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引用次数: 0
The Knowns and Unknowns of Herpesvirus Nuclear Egress. 疱疹病毒核出口的已知与未知。
IF 11.3 1区 医学 Q1 VIROLOGY Pub Date : 2023-09-29 Epub Date: 2023-04-11 DOI: 10.1146/annurev-virology-111821-105518
Barbara G Klupp, Thomas C Mettenleiter

Nuclear egress of herpesvirus capsids across the intact nuclear envelope is an exceptional vesicle-mediated nucleocytoplasmic translocation resulting in the delivery of herpesvirus capsids into the cytosol. Budding of the (nucleo)capsid at and scission from the inner nuclear membrane (INM) is mediated by the viral nuclear egress complex (NEC) resulting in a transiently enveloped virus particle in the perinuclear space followed by fusion of the primary envelope with the outer nuclear membrane (ONM). The dimeric NEC oligomerizes into a honeycomb-shaped coat underlining the INM to induce membrane curvature and scission. Mutational analyses complemented structural data defining functionally important regions. Questions remain, including where and when the NEC is formed and how membrane curvature is mediated, vesicle formation is regulated, and directionality is secured. The composition of the primary enveloped virion and the machinery mediating fusion of the primary envelope with the ONM is still debated. While NEC-mediated budding apparently follows a highly conserved mechanism, species and/or cell type-specific differences complicate understanding of later steps.

疱疹病毒衣壳穿过完整核膜的核出口是一种特殊的囊泡介导的核质易位,导致疱疹病毒衣衣壳进入胞质溶胶。病毒核出口复合物(NEC)介导(核)衣壳在内核膜(INM)上出芽和从内核膜上断裂,导致核周空间中的瞬时包膜病毒颗粒,随后初级包膜与外核膜(ONM)融合。二聚体NEC低聚成蜂窝状涂层,在INM下面,以诱导膜弯曲和断裂。突变分析补充了定义功能重要区域的结构数据。问题仍然存在,包括NEC在哪里和何时形成,以及如何介导膜弯曲,调节囊泡形成,以及确保方向性。初级包膜病毒粒子的组成以及介导初级包膜与ONM融合的机制仍存在争议。虽然NEC介导的出芽明显遵循高度保守的机制,但物种和/或细胞类型的特异性差异使对后续步骤的理解复杂化。
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引用次数: 3
Structures and Mechanisms of Nonsegmented, Negative-Strand RNA Virus Polymerases. 非分段负链RNA病毒聚合酶的结构和机制。
IF 11.3 1区 医学 Q1 VIROLOGY Pub Date : 2023-09-29 Epub Date: 2023-05-03 DOI: 10.1146/annurev-virology-111821-102603
Mohamed Ouizougun-Oubari, Rachel Fearns

The nonsegmented, negative-strand RNA viruses (nsNSVs), also known as the order Mononegavirales, have a genome consisting of a single strand of negative-sense RNA. Integral to the nsNSV replication cycle is the viral polymerase, which is responsible for transcribing the viral genome, to produce an array of capped and polyadenylated messenger RNAs, and replicating it to produce new genomes. To perform the different steps that are necessary for these processes, the nsNSV polymerases undergo a series of coordinated conformational transitions. While much is still to be learned regarding the intersection of nsNSV polymerase dynamics, structure, and function, recently published polymerase structures, combined with a history of biochemical and molecular biology studies, have provided new insights into how nsNSV polymerases function as dynamic machines. In this review, we consider each of the steps involved in nsNSV transcription and replication and suggest how these relate to solved polymerase structures.

非片段负链RNA病毒(nsNSV),也称为单阴性病毒目,其基因组由单链负义RNA组成。nsNSV复制周期中不可或缺的是病毒聚合酶,它负责转录病毒基因组,产生一系列带帽和多腺苷酸化的信使RNA,并将其复制以产生新的基因组。为了进行这些过程所需的不同步骤,nsNSV聚合酶经历一系列配位构象转变。尽管关于nsNSV聚合酶动力学、结构和功能的交叉还有很多需要了解,但最近发表的聚合酶结构,结合生物化学和分子生物学研究的历史,为nsNSV多聚酶如何作为动态机器发挥作用提供了新的见解。在这篇综述中,我们考虑了nsNSV转录和复制所涉及的每一个步骤,并提出了这些步骤与已解决的聚合酶结构的关系。
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引用次数: 3
Structure and Role of O-Linked Glycans in Viral Envelope Proteins. O-连接的甘氨酸在病毒包膜蛋白中的结构和作用。
IF 11.3 1区 医学 Q1 VIROLOGY Pub Date : 2023-09-29 Epub Date: 2023-07-06 DOI: 10.1146/annurev-virology-111821-121007
Sigvard Olofsson, Marta Bally, Edward Trybala, Tomas Bergström

N- and O-glycans are both important constituents of viral envelope glycoproteins. O-linked glycosylation can be initiated by any of 20 different human polypeptide O-acetylgalactosaminyl transferases, resulting in an important functional O-glycan heterogeneity. O-glycans are organized as solitary glycans or in clusters of multiple glycans forming mucin-like domains. They are functional both in the viral life cycle and in viral colonization of their host. Negatively charged O-glycans are crucial for the interactions between glycosaminoglycan-binding viruses and their host. A novel mechanism, based on controlled electrostatic repulsion, explains how such viruses solve the conflict between optimized viral attachment to target cells and efficient egress of progeny virus. Conserved solitary O-glycans appear important for viral uptake in target cells by contributing to viral envelope fusion. Dual roles of viral O-glycans in the host B cell immune response, either epitope blocking or epitope promoting, may be exploitable for vaccine development. Finally, specific virus-induced O-glycans may be involved in viremic spread.

N-和O-聚糖都是病毒包膜糖蛋白的重要组成部分。O-连接的糖基化可以由20种不同的人类多肽O-乙酰氨基半乳糖转移酶中的任何一种启动,导致重要的功能O-聚糖异质性。O-聚糖被组织为单独的聚糖或形成粘蛋白样结构域的多个聚糖的簇。它们在病毒生命周期和宿主的病毒定殖中都具有功能。带负电荷的O-聚糖对糖胺聚糖结合病毒与其宿主之间的相互作用至关重要。一种基于可控静电排斥的新机制解释了这种病毒如何解决病毒与靶细胞的最佳附着和子代病毒的有效排出之间的冲突。保存的孤立O-聚糖通过促进病毒包膜融合,对靶细胞中的病毒摄取似乎很重要。病毒O-聚糖在宿主B细胞免疫反应中的双重作用,即表位阻断或表位促进,可能可用于疫苗开发。最后,特定病毒诱导的O-聚糖可能参与病毒血症的传播。
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引用次数: 1
CBASS to cGAS-STING: The Origins and Mechanisms of Nucleotide Second Messenger Immune Signaling. CBASS至cGAS STING:核苷酸第二信使免疫信号的起源和机制。
IF 11.3 1区 医学 Q1 VIROLOGY Pub Date : 2023-09-29 Epub Date: 2023-06-28 DOI: 10.1146/annurev-virology-111821-115636
Kailey M Slavik, Philip J Kranzusch

Host defense against viral pathogens is an essential function for all living organisms. In cell-intrinsic innate immunity, dedicated sensor proteins recognize molecular signatures of infection and communicate to downstream adaptor or effector proteins to activate immune defense. Remarkably, recent evidence demonstrates that much of the core machinery of innate immunity is shared across eukaryotic and prokaryotic domains of life. Here, we review a pioneering example of evolutionary conservation in innate immunity: the animal cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon genes) signaling pathway and its ancestor in bacteria, CBASS (cyclic nucleotide-based antiphage signaling system) antiphage defense. We discuss the unique mechanism by which animal cGLRs (cGAS-like receptors) and bacterial CD-NTases (cGAS/dinucleotide-cyclase in Vibrio (DncV)-like nucleotidyltransferases) in these pathways link pathogen detection with immune activation using nucleotide second messenger signals. Comparing the biochemical, structural, and mechanistic details of cGAS-STING, cGLR signaling, and CBASS, we highlight emerging questions in the field and examine evolutionary pressures that may have shaped the origins of nucleotide second messenger signaling in antiviral defense.

宿主防御病毒病原体是所有生物体的基本功能。在细胞固有先天免疫中,专用传感器蛋白识别感染的分子特征,并与下游衔接蛋白或效应蛋白通信,以激活免疫防御。值得注意的是,最近的证据表明,先天免疫的大部分核心机制在真核生物和原核生物的生命领域中是共享的。在这里,我们回顾了先天免疫进化保护的一个开创性例子:动物cGAS-STING(干扰素基因的环状GMP-AMP合酶刺激因子)信号通路及其在细菌中的祖先,CBASS(基于环核苷酸的抗噬菌体信号系统)抗噬菌体防御。我们讨论了动物cGLRs(cGAS样受体)和细菌CD NTase(Vibrio(DncV)样核苷酸转移酶中的cGAS/二核苷酸环化酶)在这些途径中使用核苷酸第二信使信号将病原体检测与免疫激活联系起来的独特机制。比较cGAS STING、cGLR信号传导和CBASS的生化、结构和机制细节,我们强调了该领域新出现的问题,并研究了可能影响抗病毒防御中核苷酸第二信使信号传导起源的进化压力。
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引用次数: 4
What Have We Learned by Resurrecting the 1918 Influenza Virus? 我们从1918年流感病毒的复活中学到了什么?
IF 11.3 1区 医学 Q1 VIROLOGY Pub Date : 2023-09-29 DOI: 10.1146/annurev-virology-111821-104408
Brad Gilbertson, Kanta Subbarao

The 1918 Spanish influenza pandemic was one of the deadliest infectious disease events in recorded history, resulting in approximately 50-100 million deaths worldwide. The origins of the 1918 virus and the molecular basis for its exceptional virulence remained a mystery for much of the 20th century because the pandemic predated virologic techniques to isolate, passage, and store influenza viruses. In the late 1990s, overlapping fragments of influenza viral RNA preserved in the tissues of several 1918 victims were amplified and sequenced. The use of influenza reverse genetics then permitted scientists to reconstruct the 1918 virus entirely from cloned complementary DNA, leading to new insights into the origin of the virus and its pathogenicity. Here, we discuss some of the advances made by resurrection of the 1918 virus, including the rise of innovative molecular research, which is a topic in the dual use debate.

1918年西班牙流感大流行是有记录以来最致命的传染病事件之一,导致全球约5000万至1亿人死亡。1918年病毒的起源及其异常毒力的分子基础在20世纪的大部分时间里仍然是个谜,因为这场大流行早于分离、传播和储存流感病毒的病毒学技术。20世纪90年代末,保存在1918名受害者组织中的流感病毒RNA的重叠片段被扩增并测序。流感反向遗传学的使用使科学家能够完全从克隆的互补DNA中重建1918年的病毒,从而对病毒的起源及其致病性有了新的见解。在这里,我们讨论1918年病毒复活所取得的一些进展,包括创新分子研究的兴起,这是两用辩论中的一个话题。
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引用次数: 0
The Times They Are a-Changing. 时代在改变。
IF 11.3 1区 医学 Q1 VIROLOGY Pub Date : 2023-09-29 DOI: 10.1146/annurev-vi-10-102822-100111
Lynn W Enquist
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引用次数: 0
For Better or Worse: Modulation of the Host DNA Damage Response by Human Papillomavirus. 好与坏:人类乳头瘤病毒对宿主DNA损伤反应的调节。
IF 11.3 1区 医学 Q1 VIROLOGY Pub Date : 2023-09-29 Epub Date: 2023-04-11 DOI: 10.1146/annurev-virology-111821-103452
Caleb J Studstill, Cary A Moody

High-risk human papillomaviruses (HPVs) are associated with several human cancers. HPVs are small, DNA viruses that rely on host cell machinery for viral replication. The HPV life cycle takes place in the stratified epithelium, which is composed of different cell states, including terminally differentiating cells that are no longer active in the cell cycle. HPVs have evolved mechanisms to persist and replicate in the stratified epithelium by hijacking and modulating cellular pathways, including the DNA damage response (DDR). HPVs activate and exploit DDR pathways to promote viral replication, which in turn increases the susceptibility of the host cell to genomic instability and carcinogenesis. Here, we review recent advances in our understanding of the regulation of the host cell DDR by high-risk HPVs during the viral life cycle and discuss the potential cellular consequences of modulating DDR pathways.

高危型人乳头瘤病毒(HPV)与几种人类癌症有关。HPV是一种小型DNA病毒,依靠宿主细胞机制进行病毒复制。HPV的生命周期发生在复层上皮中,复层上皮由不同的细胞状态组成,包括在细胞周期中不再活跃的终末分化细胞。HPV已经进化出通过劫持和调节细胞途径(包括DNA损伤反应(DDR))在复层上皮中持续和复制的机制。HPV激活并利用DDR途径促进病毒复制,从而增加宿主细胞对基因组不稳定和致癌的易感性。在这里,我们回顾了我们对高风险HPV在病毒生命周期中调节宿主细胞DDR的理解的最新进展,并讨论了调节DDR途径的潜在细胞后果。
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引用次数: 0
期刊
Annual Review of Virology
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