Capsid protein structure, self-assembly, and processing reveal morphogenesis of the marine virophage mavirus

Born, D.; Reuter, L.; Mersdorf, Ulrike; Mueller, Melanie; Fischer, Matthias; Meinhart, Anton; Reinstein, Jochen

doi:10.1073/pnas.1805376115

Cited by 18 publications

(23 citation statements)

References 43 publications

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“…Several other virophages, as well as a large number of virophage candidates, have been identified since then 195,198,200 . Recent studies show that virophages could resemble bona fide DNA viruses 201 and their reclassification as their own viral family has been proposed 195 .…”

Section: Box 1 | the Expanding Family Of Sub-viral Particlesmentioning

confidence: 99%

Defective viral genomes are key drivers of the virus–host interaction

2019

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Viruses survive often harsh host environments, yet we know little about the strategies they utilize to adapt and subsist given their limited genomic resources. We are beginning to appreciate the surprising versatility of viral genomes and how replicationcompetent and -defective virus variants can provide means for adaptation, immune escape and virus perpetuation. This Review summarizes current knowledge of the types of defective viral genomes generated during the replication of RNA viruses and the functions that they carry out. We highlight the universality and diversity of defective viral genomes during infections and discuss their predicted role in maintaining a fit virus population, their impact on human and animal health, and their potential to be harnessed as antiviral tools. Review ARticleNATuRe MicRoBiology extinction interfere with replication of a wild-type viral genome 29,30 . Hypermutations and mutations leading to frame shifts also result in defective viruses 31 (Fig. 1a). One example is mutations introduced by the cellular protein APOBEC3G into pro-retroviruses 32 . APOBEC3G deaminates deoxycytidine nucleotides in the viral DNA, leading to hypermutations that interfere with the ability of the viral genome to integrate into the host genome and replicate. Interestingly, in opposition to an interfering activity for these mutated pro-viruses, it has been proposed that defective proviruses enhance fitness and that complementation among them drives viral persistence and pathogenesis 33,34 .Deletions. The genomic viral species most commonly referred to as DVGs are truncated viral genomes resulting from large internal deletions occurring during viral replication. Deletion DVGs tend to bear single large truncations that remove several or all essential genes required for self-propagation while retaining 5′ and 3′ ends as well as other RNA structural elements required for polymerase binding, replication and/or packaging [35][36][37] . Multiple variants also exist, including DVGs that can be described as 'mosaic' in that they appear to be the result of multiple recombination and rearrangement events, including deletions, insertions, duplications and even inversions of parts of the genome [38][39][40] (Fig. 1b). Copy-backs.Copy-back and snap-back DVGs are rearranged genomes in which a sequence is duplicated in reverse complement to create theoretical stem-like structures (panhandle structures for copy-back DVGs or hairpin structures for snap-back DVGs) 41-43 . Copy-back DVGs have been reported in many negative-sense (ns) RNA viruses and are generated from the 5′ end of the genome in a process that produces DVGs with complementary 3′ and 5′ termini 44,45 . If the complementary region of the DVG comprises almost the entire sequence, the DVG can be further characterized as a snap-back DVG 43 (Fig. 1c). Copy-back DVGs are predicted to be generated when the viral RNA-dependent RNA polymerase (RdRP) detaches from the template and reattaches to the nascent strand, copying back the end of the genome 42,46 .

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Section: Box 1 | the Expanding Family Of Sub-viral Particlesmentioning

confidence: 99%

Defective viral genomes are key drivers of the virus–host interaction

2019

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“…Once inside the cell, the viral DNA must gain access to the nucleus in order to achieve host genome integration. A nuclear localization signal (NLS) is predicted in the mavirus major capsid and MV13 proteins, which could thus be involved in nuclear transport . These two proteins are virion components, implying that the capsid itself (or parts thereof) could translocate to the nucleus.…”

Section: Evidence For Virophage Genome Integrationmentioning

confidence: 99%

“…A nuclear localization signal (NLS) is predicted in the mavirus major capsid and MV13 proteins, which could thus be involved in nuclear transport. 38 These two proteins are virion components, implying that the capsid itself (or parts thereof) could translocate to the nucleus. Alternatively, the rve-INT or another virophage genome-bound protein could mediate nuclear import.…”

Section: Evidence For Virophage Genome Integrationmentioning

confidence: 99%

“…In contrast, mavirus enters the host cell independently of its giant virus CroV and thus can integrate in healthy cells. Because the rve‐INT protein is packaged within the mavirus particle, its activity should not depend on de novo transcription, which has so far only been observed in the presence of CroV. Once inside the cell, the viral DNA must gain access to the nucleus in order to achieve host genome integration.…”

Section: Evidence For Virophage Genome Integrationmentioning

confidence: 99%

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The dual lifestyle of genome‐integrating virophages in protists

Berjón-Otero

Koslová

Fischer

2019

Annals of the New York Academy of Sciences

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DNA viruses with efficient host genome integration capability were unknown in eukaryotes until recently. The discovery of virophages, satellite‐like DNA viruses that depend on lytic giant viruses that infect protists, revealed a genetically diverse group of viruses with high genome mobility. Virophages can act as strong inhibitors of their associated giant viruses, and the resulting beneficial effects on their unicellular hosts resemble a population‐based antiviral defense mechanism. By comparing various aspects of genome‐integrating virophages, in particular the virophage mavirus, with other mobile genetic elements and parasite‐derived defense mechanisms in eukaryotes and prokaryotes, we show that virophages share many features with other host–parasite systems. Yet, the dual lifestyle exhibited by mavirus remains unprecedented among eukaryotic DNA viruses, with potentially far‐reaching ecological and evolutionary consequences for the host.

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“…The core double β-barrel is key for assembling the pseudo-hexameric capsomers, the elemental building blocks for generating virions with increasing sizes ( Figure 1 C). The interior-module allows the rotational registering across capsomers and the anchoring of the capsomers to the underneath structural constituents and, depending on the virus type, to the membrane vesicle, to membrane-associated proteins, or to the genome ( Figure 1 B, left) [ 27 , 28 , 29 , 57 ]. The exterior module, constituted by the turret domains or extended loops above the V1 and V2 towers, is also in some cases, such as adenovirus hexon, faustovirus and ASFV p72 MCPs, involved in trimer/capsomer stabilization [ 22 , 33 , 53 ].…”

Section: Major Capsid Proteins With a Double β-Barrel Fold: The Comentioning

confidence: 99%

Superimposition of Viral Protein Structures: A Means to Decipher the Phylogenies of Viruses

Ravantti

Martínez-Castillo

Abrescia

2020

Viruses

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Superimposition of protein structures is key in unravelling structural homology across proteins whose sequence similarity is lost. Structural comparison provides insights into protein function and evolution. Here, we review some of the original findings and thoughts that have led to the current established structure-based phylogeny of viruses: starting from the original observation that the major capsid proteins of plant and animal viruses possess similar folds, to the idea that each virus has an innate “self”. This latter idea fueled the conceptualization of the PRD1-adenovirus lineage whose members possess a major capsid protein (innate “self”) with a double jelly roll fold. Based on this approach, long-range viral evolutionary relationships can be detected allowing the virosphere to be classified in four structure-based lineages. However, this process is not without its challenges or limitations. As an example of these hurdles, we finally touch on the difficulty of establishing structural “self” traits for enveloped viruses showcasing the coronaviruses but also the power of structure-based analysis in the understanding of emerging viruses

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Capsid protein structure, self-assembly, and processing reveal morphogenesis of the marine virophage mavirus

Cited by 18 publications

References 43 publications

Defective viral genomes are key drivers of the virus–host interaction

Defective viral genomes are key drivers of the virus–host interaction

The dual lifestyle of genome‐integrating virophages in protists

Superimposition of Viral Protein Structures: A Means to Decipher the Phylogenies of Viruses

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