Pub Date : 2022-09-29Epub Date: 2022-06-07DOI: 10.1146/annurev-virology-100120-012345
Léa Gaucherand, Marta Maria Gaglia
Many viruses induce shutoff of host gene expression (host shutoff) as a strategy to take over cellular machinery and evade host immunity. Without host shutoff activity, these viruses generally replicate poorly in vivo, attesting to the importance of this antiviral strategy. In this review, we discuss one particularly advantageous way for viruses to induce host shutoff: triggering widespread host messenger RNA (mRNA) decay. Viruses can trigger increased mRNA destruction either directly, by encoding RNA cleaving or decapping enzymes, or indirectly, by activating cellular RNA degradation pathways. We review what is known about the mechanism of action of several viral RNA degradation factors. We then discuss the consequences of widespread RNA degradation on host gene expression and on the mechanisms of immune evasion, highlighting open questions. Answering these questions is critical to understanding how viral RNA degradation factors regulate host gene expression and how this process helps viruses evade host responses and replicate.
{"title":"The Role of Viral RNA Degrading Factors in Shutoff of Host Gene Expression.","authors":"Léa Gaucherand, Marta Maria Gaglia","doi":"10.1146/annurev-virology-100120-012345","DOIUrl":"https://doi.org/10.1146/annurev-virology-100120-012345","url":null,"abstract":"<p><p>Many viruses induce shutoff of host gene expression (host shutoff) as a strategy to take over cellular machinery and evade host immunity. Without host shutoff activity, these viruses generally replicate poorly in vivo, attesting to the importance of this antiviral strategy. In this review, we discuss one particularly advantageous way for viruses to induce host shutoff: triggering widespread host messenger RNA (mRNA) decay. Viruses can trigger increased mRNA destruction either directly, by encoding RNA cleaving or decapping enzymes, or indirectly, by activating cellular RNA degradation pathways. We review what is known about the mechanism of action of several viral RNA degradation factors. We then discuss the consequences of widespread RNA degradation on host gene expression and on the mechanisms of immune evasion, highlighting open questions. Answering these questions is critical to understanding how viral RNA degradation factors regulate host gene expression and how this process helps viruses evade host responses and replicate.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2022-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9530000/pdf/nihms-1819195.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41178957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-09-29DOI: 10.1146/annurev-virology-100220-113942
Mette M Rosenkilde, Naotaka Tsutsumi, Julius M Knerr, Dagmar F Kildedal, K Christopher Garcia
Herpesviruses are ancient large DNA viruses that have exploited gene capture as part of their strategy to escape immune surveillance, promote virus spreading, or reprogram host cells to benefit their survival. Most acquired genes are transmembrane proteins and cytokines, such as viral G protein-coupled receptors (vGPCRs), chemokines, and chemokine-binding proteins. This review focuses on the vGPCRs encoded by the human β- and γ-herpesviruses. These include receptors from human cytomegalovirus, which encodes four vGPCRs: US27, US28, UL33, and UL78; human herpesvirus 6 and 7 with two receptors: U12 and U51; Epstein-Barr virus with one: BILF1; and Kaposi's sarcoma-associated herpesvirus with one: open reading frame 74, ORF74. We discuss ligand binding, signaling, and structures of the vGPCRs in light of robust differences from endogenous receptors. Finally, we briefly discuss the therapeutic targeting of vGPCRs as future treatment of acute and chronic herpesvirus infections.
{"title":"Viral G Protein-Coupled Receptors Encoded by β- and γ-Herpesviruses.","authors":"Mette M Rosenkilde, Naotaka Tsutsumi, Julius M Knerr, Dagmar F Kildedal, K Christopher Garcia","doi":"10.1146/annurev-virology-100220-113942","DOIUrl":"https://doi.org/10.1146/annurev-virology-100220-113942","url":null,"abstract":"<p><p>Herpesviruses are ancient large DNA viruses that have exploited gene capture as part of their strategy to escape immune surveillance, promote virus spreading, or reprogram host cells to benefit their survival. Most acquired genes are transmembrane proteins and cytokines, such as viral G protein-coupled receptors (vGPCRs), chemokines, and chemokine-binding proteins. This review focuses on the vGPCRs encoded by the human β- and γ-herpesviruses. These include receptors from human cytomegalovirus, which encodes four vGPCRs: US27, US28, UL33, and UL78; human herpesvirus 6 and 7 with two receptors: U12 and U51; Epstein-Barr virus with one: BILF1; and Kaposi's sarcoma-associated herpesvirus with one: open reading frame 74, ORF74. We discuss ligand binding, signaling, and structures of the vGPCRs in light of robust differences from endogenous receptors. Finally, we briefly discuss the therapeutic targeting of vGPCRs as future treatment of acute and chronic herpesvirus infections.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2022-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9584139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9201509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-09-29DOI: 10.1146/annurev-virology-100520-114412
Svetlana Y Folimonova, Yong-Duo Sun
Citrus tristeza virus (CTV) is the most destructive viral pathogen of citrus. During the past century, CTV induced grave epidemics in citrus-growing areas worldwide that have resulted in a loss of more than 100 million trees. At present, the virus continues to threaten citrus production in many different countries. Research on CTV is accompanied by distinctive challenges stemming from the large size of its RNA genome, the narrow host range limited to slow-growing Citrus species and relatives, and the complexity of CTV populations. Despite these hurdles, remarkable progress has been made in understanding the CTV-host interactions and in converting the virus into a tool for crop protection and improvement. This review focuses on recent advances that have shed light on the mechanisms underlying CTV infection. Understanding these mechanisms is pivotal for the development of means to control CTV diseases and, ultimately, turn this virus into an ally.
{"title":"<i>Citrus Tristeza Virus</i>: From Pathogen to Panacea.","authors":"Svetlana Y Folimonova, Yong-Duo Sun","doi":"10.1146/annurev-virology-100520-114412","DOIUrl":"https://doi.org/10.1146/annurev-virology-100520-114412","url":null,"abstract":"<p><p><i>Citrus tristeza virus</i> (CTV) is the most destructive viral pathogen of citrus. During the past century, CTV induced grave epidemics in citrus-growing areas worldwide that have resulted in a loss of more than 100 million trees. At present, the virus continues to threaten citrus production in many different countries. Research on CTV is accompanied by distinctive challenges stemming from the large size of its RNA genome, the narrow host range limited to slow-growing <i>Citrus</i> species and relatives, and the complexity of CTV populations. Despite these hurdles, remarkable progress has been made in understanding the CTV-host interactions and in converting the virus into a tool for crop protection and improvement. This review focuses on recent advances that have shed light on the mechanisms underlying CTV infection. Understanding these mechanisms is pivotal for the development of means to control CTV diseases and, ultimately, turn this virus into an ally.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2022-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10409018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-09-29DOI: 10.1146/annurev-virology-093020-015957
Jennifer Wirth, Mark Young
Over the past 20 years, our knowledge of virus diversity and abundance in subsurface environments has expanded dramatically through application of quantitative metagenomic approaches. In most subsurface environments, viral diversity and abundance rival viral diversity and abundance observed in surface environments. Most of these viruses are uncharacterized in terms of their hosts and replication cycles. Analysis of accessory metabolic genes encoded by subsurface viruses indicates that they evolved to replicate within the unique features of their environments. The key question remains: What role do these viruses play in the ecology and evolution of the environments in which they replicate? Undoubtedly, as more virologists examine the role of viruses in subsurface environments, new insights will emerge.
{"title":"Viruses in Subsurface Environments.","authors":"Jennifer Wirth, Mark Young","doi":"10.1146/annurev-virology-093020-015957","DOIUrl":"https://doi.org/10.1146/annurev-virology-093020-015957","url":null,"abstract":"<p><p>Over the past 20 years, our knowledge of virus diversity and abundance in subsurface environments has expanded dramatically through application of quantitative metagenomic approaches. In most subsurface environments, viral diversity and abundance rival viral diversity and abundance observed in surface environments. Most of these viruses are uncharacterized in terms of their hosts and replication cycles. Analysis of accessory metabolic genes encoded by subsurface viruses indicates that they evolved to replicate within the unique features of their environments. The key question remains: What role do these viruses play in the ecology and evolution of the environments in which they replicate? Undoubtedly, as more virologists examine the role of viruses in subsurface environments, new insights will emerge.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2022-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40383122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-06-15DOI: 10.1146/annurev-virology-100120-015057
E. Holmes
The coronavirus disease 2019 (COVID-19) pandemic has had a profound impact on human health, economic well-being, and societal function. It is essential that we use this generational experience to better understand the processes that underpin the emergence of COVID-19 and other zoonotic diseases. Herein, I review the mechanisms that determine why and how viruses emerge in new hosts, as well as the barriers to this process. I show that traditional studies of virus emergence have an inherent anthropocentric bias, with disease in humans considered the inevitable outcome of virus emergence, when in reality viruses are integral components of a global ecosystem characterized by continual host jumping with humans also transmitting their viruses to other animals. I illustrate these points using coronaviruses, including severe acute respiratory syndrome coronavirus 2, as a case study. I also outline the potential steps that can be followed to help mitigate and prevent future pandemics, with combating climate change a central component. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
{"title":"The Ecology of Viral Emergence.","authors":"E. Holmes","doi":"10.1146/annurev-virology-100120-015057","DOIUrl":"https://doi.org/10.1146/annurev-virology-100120-015057","url":null,"abstract":"The coronavirus disease 2019 (COVID-19) pandemic has had a profound impact on human health, economic well-being, and societal function. It is essential that we use this generational experience to better understand the processes that underpin the emergence of COVID-19 and other zoonotic diseases. Herein, I review the mechanisms that determine why and how viruses emerge in new hosts, as well as the barriers to this process. I show that traditional studies of virus emergence have an inherent anthropocentric bias, with disease in humans considered the inevitable outcome of virus emergence, when in reality viruses are integral components of a global ecosystem characterized by continual host jumping with humans also transmitting their viruses to other animals. I illustrate these points using coronaviruses, including severe acute respiratory syndrome coronavirus 2, as a case study. I also outline the potential steps that can be followed to help mitigate and prevent future pandemics, with combating climate change a central component. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2022-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41997129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-06-15DOI: 10.1146/annurev-virology-100520-014520
A. Creager
The history of tobacco mosaic virus (TMV) includes many firsts in science, beginning with its being the first virus identified. This review offers an overview of a history of research on TMV, with an emphasis on its close connections to the emergence and development of molecular biology. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
{"title":"Tobacco Mosaic Virus and the History of Molecular Biology.","authors":"A. Creager","doi":"10.1146/annurev-virology-100520-014520","DOIUrl":"https://doi.org/10.1146/annurev-virology-100520-014520","url":null,"abstract":"The history of tobacco mosaic virus (TMV) includes many firsts in science, beginning with its being the first virus identified. This review offers an overview of a history of research on TMV, with an emphasis on its close connections to the emergence and development of molecular biology. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2022-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46036709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-06-15DOI: 10.1146/annurev-virology-020922-110929
Thorsten G. Müller, V. Zila, B. Müller, H. Kräusslich
After cell entry, human immunodeficiency virus type 1 (HIV-1) replication involves reverse transcription of the RNA genome, nuclear import of the subviral complex without nuclear envelope breakdown, and integration of the viral complementary DNA into the host genome. Here, we discuss recent evidence indicating that completion of reverse transcription and viral genome uncoating occur in the nucleus rather than in the cytoplasm, as previously thought, and suggest a testable model for nuclear import and uncoating. Multiple recent studies indicated that the cone-shaped capsid, which encases the genome and replication proteins, not only serves as a reaction container for reverse transcription and as a shield from innate immune sensors but also may constitute the elusive HIV-1 nuclear import factor. Rupture of the capsid may be triggered in the nucleus by completion of reverse transcription, by yet-unknown nuclear factors, or by physical damage, and it appears to occur in close temporal and spatial association with the integration process. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
{"title":"Nuclear Capsid Uncoating and Reverse Transcription of HIV-1.","authors":"Thorsten G. Müller, V. Zila, B. Müller, H. Kräusslich","doi":"10.1146/annurev-virology-020922-110929","DOIUrl":"https://doi.org/10.1146/annurev-virology-020922-110929","url":null,"abstract":"After cell entry, human immunodeficiency virus type 1 (HIV-1) replication involves reverse transcription of the RNA genome, nuclear import of the subviral complex without nuclear envelope breakdown, and integration of the viral complementary DNA into the host genome. Here, we discuss recent evidence indicating that completion of reverse transcription and viral genome uncoating occur in the nucleus rather than in the cytoplasm, as previously thought, and suggest a testable model for nuclear import and uncoating. Multiple recent studies indicated that the cone-shaped capsid, which encases the genome and replication proteins, not only serves as a reaction container for reverse transcription and as a shield from innate immune sensors but also may constitute the elusive HIV-1 nuclear import factor. Rupture of the capsid may be triggered in the nucleus by completion of reverse transcription, by yet-unknown nuclear factors, or by physical damage, and it appears to occur in close temporal and spatial association with the integration process. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2022-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43980515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-06-08DOI: 10.1146/annurev-virology-091919-072546
E. Taks, S. Moorlag, M. Netea, J. van der Meer
Trained immunity is defined as the de facto memory characteristics induced in innate immune cells after exposure to microbial stimuli after infections or certain types of vaccines. Through epigenetic and metabolic reprogramming of innate immune cells after exposure to these stimuli, trained immunity induces an enhanced nonspecific protection by improving the inflammatory response upon restimulation with the same or different pathogens. Recent studies have increasingly shown that trained immunity can, on the one hand, be induced by exposure to viruses; on the other hand, when induced, it can also provide protection against heterologous viral infections. In this review we explore current knowledge on trained immunity and its relevance for viral infections, as well as its possible future uses. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
{"title":"Shifting the Immune Memory Paradigm: Trained Immunity in Viral Infections.","authors":"E. Taks, S. Moorlag, M. Netea, J. van der Meer","doi":"10.1146/annurev-virology-091919-072546","DOIUrl":"https://doi.org/10.1146/annurev-virology-091919-072546","url":null,"abstract":"Trained immunity is defined as the de facto memory characteristics induced in innate immune cells after exposure to microbial stimuli after infections or certain types of vaccines. Through epigenetic and metabolic reprogramming of innate immune cells after exposure to these stimuli, trained immunity induces an enhanced nonspecific protection by improving the inflammatory response upon restimulation with the same or different pathogens. Recent studies have increasingly shown that trained immunity can, on the one hand, be induced by exposure to viruses; on the other hand, when induced, it can also provide protection against heterologous viral infections. In this review we explore current knowledge on trained immunity and its relevance for viral infections, as well as its possible future uses. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2022-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47164869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-06-07DOI: 10.1146/annurev-virology-100220-112915
M. Stenglein
Virology has largely focused on viruses that are pathogenic to humans or to the other species that we care most about. There is no doubt that this has been a worthwhile investment. But many transformative advances have been made through the in-depth study of relatively obscure viruses that do not appear on lists of prioritized pathogens. In this review, I highlight the benefits that can accrue from the study of viruses and hosts off the beaten track. I take stock of viral sequence diversity across host taxa as an estimate of the bias that exists in our understanding of host-virus interactions. I describe the gains that have been made through the metagenomic discovery of thousands of new viruses in previously unsampled hosts as well as the limitations of metagenomic surveys. I conclude by suggesting that the study of viruses that naturally infect existing and emerging model organisms represents an opportunity to push virology forward in useful and hard to predict ways.Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
{"title":"The Case for Studying New Viruses of New Hosts.","authors":"M. Stenglein","doi":"10.1146/annurev-virology-100220-112915","DOIUrl":"https://doi.org/10.1146/annurev-virology-100220-112915","url":null,"abstract":"Virology has largely focused on viruses that are pathogenic to humans or to the other species that we care most about. There is no doubt that this has been a worthwhile investment. But many transformative advances have been made through the in-depth study of relatively obscure viruses that do not appear on lists of prioritized pathogens. In this review, I highlight the benefits that can accrue from the study of viruses and hosts off the beaten track. I take stock of viral sequence diversity across host taxa as an estimate of the bias that exists in our understanding of host-virus interactions. I describe the gains that have been made through the metagenomic discovery of thousands of new viruses in previously unsampled hosts as well as the limitations of metagenomic surveys. I conclude by suggesting that the study of viruses that naturally infect existing and emerging model organisms represents an opportunity to push virology forward in useful and hard to predict ways.Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2022-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42517266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-05-24DOI: 10.1146/annurev-virology-092920-021307
M. Nishikiori, J. D. den Boon, Nuruddin Unchwaniwala, P. Ahlquist
Positive-strand RNA viruses, the largest genetic class of eukaryotic viruses, include coronaviruses and many other established and emerging pathogens. A major target for understanding and controlling these viruses is their genome replication, which occurs in virus-induced membrane vesicles that organize replication steps and protect double-stranded RNA intermediates from innate immune recognition. The structure of these complexes has been greatly illuminated by recent cryo-electron microscope tomography studies with several viruses. One key finding in diverse systems is the organization of crucial viral RNA replication factors in multimeric rings or crowns that among other functions serve as exit channels gating release of progeny genomes to the cytosol for translation and encapsidation. Emerging results suggest that these crowns serve additional important purposes in replication complex assembly, function, and interaction with downstream processes such as encapsidation. The findings provide insights into viral function and evolution and new bases for understanding, controlling, and engineering positive-strand RNA viruses. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
{"title":"Crowning Touches in Positive-Strand RNA Virus Genome Replication Complex Structure and Function.","authors":"M. Nishikiori, J. D. den Boon, Nuruddin Unchwaniwala, P. Ahlquist","doi":"10.1146/annurev-virology-092920-021307","DOIUrl":"https://doi.org/10.1146/annurev-virology-092920-021307","url":null,"abstract":"Positive-strand RNA viruses, the largest genetic class of eukaryotic viruses, include coronaviruses and many other established and emerging pathogens. A major target for understanding and controlling these viruses is their genome replication, which occurs in virus-induced membrane vesicles that organize replication steps and protect double-stranded RNA intermediates from innate immune recognition. The structure of these complexes has been greatly illuminated by recent cryo-electron microscope tomography studies with several viruses. One key finding in diverse systems is the organization of crucial viral RNA replication factors in multimeric rings or crowns that among other functions serve as exit channels gating release of progeny genomes to the cytosol for translation and encapsidation. Emerging results suggest that these crowns serve additional important purposes in replication complex assembly, function, and interaction with downstream processes such as encapsidation. The findings provide insights into viral function and evolution and new bases for understanding, controlling, and engineering positive-strand RNA viruses. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2022-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43807803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}