Pub Date : 2024-07-08DOI: 10.1146/annurev-virology-111821-125122
John M Coffin, Mary F Kearney
Xenotropic murine leukemia virus (MLV)-related virus (XMRV) was first described in 2006 in some human prostate cancers. But it drew little attention until 2009, when it was also found, as infectious virus and as MLV-related DNA, in samples from people suffering from myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This discovery was rapidly followed by efforts of the international research community to understand the significance of the association and its potential to spread widely as an important human pathogen. Within a few years, efforts by researchers worldwide failed to repeat these findings, and mounting evidence for laboratory contamination with mouse-derived virus and viral DNA sequences became accepted as the explanation for the initial findings. As researchers engaged in these studies, we present here a historical review of the rise and fall of XMRV as a human pathogen, and we discuss the lessons learned from these events.
2006年,人们首次在一些人类前列腺癌中发现了与异型小鼠白血病病毒(MLV)相关的病毒(XMRV)。但直到 2009 年,在肌痛性脑脊髓炎/慢性疲劳综合征(ME/CFS)患者的样本中也发现了传染性病毒和与 MLV 相关的 DNA,这才引起了人们的注意。这一发现迅速引起了国际研究界的关注,以了解这种关联的重要性及其作为一种重要人类病原体广泛传播的潜力。几年内,全球研究人员的努力都未能重复这些发现,越来越多的证据表明,小鼠源性病毒和病毒 DNA 序列造成了实验室污染,这已被公认为是对最初发现的解释。作为参与这些研究的研究人员,我们在此对 XMRV 作为人类病原体的兴衰进行了历史回顾,并讨论了从这些事件中吸取的教训。
{"title":"False Alarm: XMRV, Cancer, and Chronic Fatigue Syndrome.","authors":"John M Coffin, Mary F Kearney","doi":"10.1146/annurev-virology-111821-125122","DOIUrl":"https://doi.org/10.1146/annurev-virology-111821-125122","url":null,"abstract":"<p><p>Xenotropic murine leukemia virus (MLV)-related virus (XMRV) was first described in 2006 in some human prostate cancers. But it drew little attention until 2009, when it was also found, as infectious virus and as MLV-related DNA, in samples from people suffering from myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This discovery was rapidly followed by efforts of the international research community to understand the significance of the association and its potential to spread widely as an important human pathogen. Within a few years, efforts by researchers worldwide failed to repeat these findings, and mounting evidence for laboratory contamination with mouse-derived virus and viral DNA sequences became accepted as the explanation for the initial findings. As researchers engaged in these studies, we present here a historical review of the rise and fall of XMRV as a human pathogen, and we discuss the lessons learned from these events.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":8.1,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141560121","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 : 2024-07-02DOI: 10.1146/annurev-virology-100422-022751
Katinka Döhner, Manutea Christophe Serrero, Abel Viejo-Borbolla, Beate Sodeik
The nucleoplasm, the cytosol, the inside of virions, and again the cytosol comprise the world in which the capsids of alphaherpesviruses encounter viral and host proteins that support or limit them in performing their tasks. Here, we review the fascinating conundrum of how specific protein-protein interactions late in alphaherpesvirus infection orchestrate capsid nuclear assembly, nuclear egress, and cytoplasmic envelopment, but target incoming capsids to the nuclear pores in naive cells to inject the viral genomes into the nucleoplasm for viral transcription and replication. Multiple capsid interactions with viral and host proteins have been characterized using viral mutants and assays that reconstitute key stages of the infection cycle. Keratinocytes, fibroblasts, mucosal epithelial cells, neurons, and immune cells employ cell type-specific intrinsic and cytokine-induced resistance mechanisms to restrict several stages of the viral infection cycle. However, concomitantly, alphaherpesviruses have evolved countermeasures to ensure efficient capsid function during infection.
{"title":"A Hitchhiker's Guide Through the Cell: The World According to the Capsids of Alphaherpesviruses.","authors":"Katinka Döhner, Manutea Christophe Serrero, Abel Viejo-Borbolla, Beate Sodeik","doi":"10.1146/annurev-virology-100422-022751","DOIUrl":"https://doi.org/10.1146/annurev-virology-100422-022751","url":null,"abstract":"<p><p>The nucleoplasm, the cytosol, the inside of virions, and again the cytosol comprise the world in which the capsids of alphaherpesviruses encounter viral and host proteins that support or limit them in performing their tasks. Here, we review the fascinating conundrum of how specific protein-protein interactions late in alphaherpesvirus infection orchestrate capsid nuclear assembly, nuclear egress, and cytoplasmic envelopment, but target incoming capsids to the nuclear pores in naive cells to inject the viral genomes into the nucleoplasm for viral transcription and replication. Multiple capsid interactions with viral and host proteins have been characterized using viral mutants and assays that reconstitute key stages of the infection cycle. Keratinocytes, fibroblasts, mucosal epithelial cells, neurons, and immune cells employ cell type-specific intrinsic and cytokine-induced resistance mechanisms to restrict several stages of the viral infection cycle. However, concomitantly, alphaherpesviruses have evolved countermeasures to ensure efficient capsid function during infection.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":8.1,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141493993","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 : 2024-07-01DOI: 10.1146/annurev-virology-100422-125123
Landon J Getz, Karen L Maxwell
Bacterial viruses known as phages rely on their hosts for replication and thus have developed an intimate partnership over evolutionary time. The survival of temperate phages, which can establish a chronic infection in which their genomes are maintained in a quiescent state known as a prophage, is tightly coupled with the survival of their bacterial hosts. As a result, prophages encode a diverse antiphage defense arsenal to protect themselves and the bacterial host in which they reside from further phage infection. Similarly, the survival and success of prophage-related elements such as phage-inducible chromosomal islands are directly tied to the survival and success of their bacterial host, and they also have been shown to encode numerous antiphage defenses. Here, we describe the current knowledge of antiphage defenses encoded by prophages and prophage-related mobile genetic elements.
{"title":"Diverse Antiphage Defenses Are Widespread Among Prophages and Mobile Genetic Elements.","authors":"Landon J Getz, Karen L Maxwell","doi":"10.1146/annurev-virology-100422-125123","DOIUrl":"https://doi.org/10.1146/annurev-virology-100422-125123","url":null,"abstract":"<p><p>Bacterial viruses known as phages rely on their hosts for replication and thus have developed an intimate partnership over evolutionary time. The survival of temperate phages, which can establish a chronic infection in which their genomes are maintained in a quiescent state known as a prophage, is tightly coupled with the survival of their bacterial hosts. As a result, prophages encode a diverse antiphage defense arsenal to protect themselves and the bacterial host in which they reside from further phage infection. Similarly, the survival and success of prophage-related elements such as phage-inducible chromosomal islands are directly tied to the survival and success of their bacterial host, and they also have been shown to encode numerous antiphage defenses. Here, we describe the current knowledge of antiphage defenses encoded by prophages and prophage-related mobile genetic elements.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":8.1,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141477760","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 : 2024-06-14DOI: 10.1146/annurev-virology-100422-012608
Jorge F Guerrero, Sydney L Lesko, Edward L Evans, Nathan M Sherer
Viruses exploit key host cell factors to accomplish each individual stage of the viral replication cycle. To understand viral pathogenesis and speed the development of new antiviral strategies, high-resolution visualization of virus-host interactions is needed to define where and when these events occur within cells. Here, we review state-of-the-art live cell imaging techniques for tracking individual stages of viral life cycles, focusing predominantly on retroviruses and especially human immunodeficiency virus type 1, which is most extensively studied. We describe how visible viruses can be engineered for live cell imaging and how nonmodified viruses can, in some instances, be tracked and studied indirectly using cell biosensor systems. We summarize the ways in which live cell imaging has been used to dissect the retroviral life cycle. Finally, we discuss select challenges for the future including the need for better labeling strategies, increased resolution, and multivariate systems that will allow for the study of full viral replication cycles.
{"title":"Revealing Retroviral Life Cycles Using Visible Viruses and Live Cell Imaging.","authors":"Jorge F Guerrero, Sydney L Lesko, Edward L Evans, Nathan M Sherer","doi":"10.1146/annurev-virology-100422-012608","DOIUrl":"https://doi.org/10.1146/annurev-virology-100422-012608","url":null,"abstract":"<p><p>Viruses exploit key host cell factors to accomplish each individual stage of the viral replication cycle. To understand viral pathogenesis and speed the development of new antiviral strategies, high-resolution visualization of virus-host interactions is needed to define where and when these events occur within cells. Here, we review state-of-the-art live cell imaging techniques for tracking individual stages of viral life cycles, focusing predominantly on retroviruses and especially human immunodeficiency virus type 1, which is most extensively studied. We describe how visible viruses can be engineered for live cell imaging and how nonmodified viruses can, in some instances, be tracked and studied indirectly using cell biosensor systems. We summarize the ways in which live cell imaging has been used to dissect the retroviral life cycle. Finally, we discuss select challenges for the future including the need for better labeling strategies, increased resolution, and multivariate systems that will allow for the study of full viral replication cycles.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141321837","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 : 2024-06-14DOI: 10.1146/annurev-virology-111821-122718
Anne E Simon, Diego F Quito-Avila, Sayanta Bera
Before the very recent discovery of umbra-like viruses (ULVs), the signature defining feature of all plant RNA viruses was the encoding of specialized RNA-binding movement proteins (MPs) for transiting their RNA genomes through gated plasmodesmata to establish systemic infections. The vast majority of ULVs share umbravirus-like RNA-dependent RNA polymerases and 3'-terminal structures, but they differ by not encoding cell-to-cell and long-distance MPs and by not relying on a helper virus for trans-encapsidation and plant-to-plant transmission. The recent finding that two groups of ULVs do not necessarily encode MPs is expanding our understanding of the minimum requirements for modern plant RNA viruses. ULV CY1 from citrus uses host protein PHLOEM PROTEIN 2 (PP2) for systemic movement, and related ULVs encode a capsid protein, thereby providing an explanation for the lack of helper viruses present in many ULV-infected plants. ULVs thus resemble the first viruses that infected plants, which were likely deposited from feeding organisms and would have similarly required the use of host proteins such as PP2 to exit initially infected cells.
{"title":"Expanding the Plant Virome: Umbra-Like Viruses Use Host Proteins for Movement.","authors":"Anne E Simon, Diego F Quito-Avila, Sayanta Bera","doi":"10.1146/annurev-virology-111821-122718","DOIUrl":"https://doi.org/10.1146/annurev-virology-111821-122718","url":null,"abstract":"<p><p>Before the very recent discovery of umbra-like viruses (ULVs), the signature defining feature of all plant RNA viruses was the encoding of specialized RNA-binding movement proteins (MPs) for transiting their RNA genomes through gated plasmodesmata to establish systemic infections. The vast majority of ULVs share umbravirus-like RNA-dependent RNA polymerases and 3'-terminal structures, but they differ by not encoding cell-to-cell and long-distance MPs and by not relying on a helper virus for <i>trans</i>-encapsidation and plant-to-plant transmission. The recent finding that two groups of ULVs do not necessarily encode MPs is expanding our understanding of the minimum requirements for modern plant RNA viruses. ULV CY1 from citrus uses host protein PHLOEM PROTEIN 2 (PP2) for systemic movement, and related ULVs encode a capsid protein, thereby providing an explanation for the lack of helper viruses present in many ULV-infected plants. ULVs thus resemble the first viruses that infected plants, which were likely deposited from feeding organisms and would have similarly required the use of host proteins such as PP2 to exit initially infected cells.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141321836","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 : 2024-06-14DOI: 10.1146/annurev-vi-11-060624-100111
Julie K Pfeiffer, Terence S Dermody
{"title":"Artificial Intelligence and Scientific Reviews.","authors":"Julie K Pfeiffer, Terence S Dermody","doi":"10.1146/annurev-vi-11-060624-100111","DOIUrl":"https://doi.org/10.1146/annurev-vi-11-060624-100111","url":null,"abstract":"","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141321835","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 : 2024-06-07DOI: 10.1146/annurev-virology-100422-034124
Maija E Pollari, William W E Aspelin, Linping Wang, Kristiina M Mäkinen
The negative effects of potyvirus diseases on the agricultural industry are extensive and global. Understanding how protein-protein-interactions contribute to potyviral infections is imperative to developing resistant varieties that help counter the threat potyviruses pose. While many protein-protein interactions have been reported, only a fraction are essential for potyviral infection. Accumulating evidence demonstrates that potyviral infection processes are interconnected. For instance, the interaction between the eukaryotic initiation factor 4E (eIF4E) and viral protein genome-linked (VPg) is crucial for both viral translation and protecting viral RNA (vRNA). Additionally, recent evidence for open reading frames on the reverse-sense vRNA and for nonequimolar expression of viral proteins has challenged the previous polyprotein expression model. These discoveries will surely reveal more about the potyviral protein interactome. In this review, we present a synthesis of the potyviral infection cycle and discuss influential past discoveries and recent work on protein-protein interactions in various infection processes.
{"title":"The Molecular Maze of Potyviral and Host Protein Interactions.","authors":"Maija E Pollari, William W E Aspelin, Linping Wang, Kristiina M Mäkinen","doi":"10.1146/annurev-virology-100422-034124","DOIUrl":"https://doi.org/10.1146/annurev-virology-100422-034124","url":null,"abstract":"<p><p>The negative effects of potyvirus diseases on the agricultural industry are extensive and global. Understanding how protein-protein-interactions contribute to potyviral infections is imperative to developing resistant varieties that help counter the threat potyviruses pose. While many protein-protein interactions have been reported, only a fraction are essential for potyviral infection. Accumulating evidence demonstrates that potyviral infection processes are interconnected. For instance, the interaction between the eukaryotic initiation factor 4E (eIF4E) and viral protein genome-linked (VPg) is crucial for both viral translation and protecting viral RNA (vRNA). Additionally, recent evidence for open reading frames on the reverse-sense vRNA and for nonequimolar expression of viral proteins has challenged the previous polyprotein expression model. These discoveries will surely reveal more about the potyviral protein interactome. In this review, we present a synthesis of the potyviral infection cycle and discuss influential past discoveries and recent work on protein-protein interactions in various infection processes.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141288751","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 : 2024-06-07DOI: 10.1146/annurev-virology-100422-023502
Camila E Osega, Fernando J Bustos, Gloria Arriagada
Once inside host cells, retroviruses generate a double-stranded DNA copy of their RNA genomes via reverse transcription inside a viral core, and this viral DNA is subsequently integrated into the genome of the host cell. Before integration can occur, the core must cross the cell cortex, be transported through the cytoplasm, and enter the nucleus. Retroviruses have evolved different mechanisms to accomplish this journey. This review examines the various mechanisms retroviruses, especially HIV-1, have evolved to commute throughout the cell. Retroviruses cross the cell cortex while modulating actin dynamics and use microtubules as roads while connecting with microtubule-associated proteins and motors to reach the nucleus. Although a clearer picture exists for HIV-1 compared with other retroviruses, there is still much to learn about how retroviruses accomplish their commute.
一旦进入宿主细胞,逆转录病毒就会在病毒核心内通过逆转录生成其 RNA 基因组的双链 DNA 副本,然后将病毒 DNA 整合到宿主细胞的基因组中。在整合之前,病毒核心必须穿过细胞皮层,通过细胞质运输,然后进入细胞核。逆转录病毒进化出了不同的机制来完成这一过程。本综述将探讨逆转录病毒(尤其是 HIV-1)在整个细胞中进化出的各种通勤机制。逆转录病毒在调节肌动蛋白动力学的同时穿过细胞皮层,并利用微管作为道路,同时与微管相关蛋白和马达连接以到达细胞核。尽管与其他逆转录病毒相比,HIV-1 的情况更为清晰,但关于逆转录病毒如何完成其通勤,仍有许多知识需要学习。
{"title":"From Entry to the Nucleus: How Retroviruses Commute.","authors":"Camila E Osega, Fernando J Bustos, Gloria Arriagada","doi":"10.1146/annurev-virology-100422-023502","DOIUrl":"https://doi.org/10.1146/annurev-virology-100422-023502","url":null,"abstract":"<p><p>Once inside host cells, retroviruses generate a double-stranded DNA copy of their RNA genomes via reverse transcription inside a viral core, and this viral DNA is subsequently integrated into the genome of the host cell. Before integration can occur, the core must cross the cell cortex, be transported through the cytoplasm, and enter the nucleus. Retroviruses have evolved different mechanisms to accomplish this journey. This review examines the various mechanisms retroviruses, especially HIV-1, have evolved to commute throughout the cell. Retroviruses cross the cell cortex while modulating actin dynamics and use microtubules as roads while connecting with microtubule-associated proteins and motors to reach the nucleus. Although a clearer picture exists for HIV-1 compared with other retroviruses, there is still much to learn about how retroviruses accomplish their commute.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141288749","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 : 2024-06-07DOI: 10.1146/annurev-virology-100422-040919
William C Summers
The bacteriolytic character of bacteriophages was employed as antibacterial therapy almost from the time of their discovery in 1917. In the United States, phage therapy was sporadic during the 1920s and 1930s but had dwindled into obscurity by the post-WWII period. This demise of phage therapy has traditionally been attributed to the superiority of antibiotics, discovered and first used during the war years, but this explanation is complicated by the fact that phage therapy outside the United States has had a longer and more successful life, especially in the countries of Eastern Europe. This review considers another, probably synergetic factor that was specific to the medical uses of phage in the United States: the geopolitical climate fostered by the Cold War reaction against Soviet science and its associated specter, socialized medicine. This analysis suggests that even such a purely scientific matter involving bacterial viruses cannot escape social forces and political ideologies.
{"title":"The Cold War and Phage Therapy: How Geopolitics Stalled Development of Viruses as Antibacterials.","authors":"William C Summers","doi":"10.1146/annurev-virology-100422-040919","DOIUrl":"https://doi.org/10.1146/annurev-virology-100422-040919","url":null,"abstract":"<p><p>The bacteriolytic character of bacteriophages was employed as antibacterial therapy almost from the time of their discovery in 1917. In the United States, phage therapy was sporadic during the 1920s and 1930s but had dwindled into obscurity by the post-WWII period. This demise of phage therapy has traditionally been attributed to the superiority of antibiotics, discovered and first used during the war years, but this explanation is complicated by the fact that phage therapy outside the United States has had a longer and more successful life, especially in the countries of Eastern Europe. This review considers another, probably synergetic factor that was specific to the medical uses of phage in the United States: the geopolitical climate fostered by the Cold War reaction against Soviet science and its associated specter, socialized medicine. This analysis suggests that even such a purely scientific matter involving bacterial viruses cannot escape social forces and political ideologies.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141288750","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 : 2024-06-07DOI: 10.1146/annurev-virology-100422-024648
Benoit de Thoisy, Tiago Gräf, Daniel Santos Mansur, Adriana Delfraro, Claudia Nunes Duarte Dos Santos
South American ecosystems host astonishing biodiversity, with potentially great richness in viruses. However, these ecosystems have not yet been the source of any widespread, epidemic viruses. Here we explore a set of putative causes that may explain this apparent paradox. We discuss that human presence in South America is recent, beginning around 14,000 years ago; that few domestications of native species have occurred; and that successive immigration events associated with Old World virus introductions reduced the likelihood of spillovers and adaptation of local viruses into humans. Also, the diversity and ecological characteristics of vertebrate hosts might serve as protective factors. Moreover, although forest areas remained well preserved until recently, current brutal, sudden, and large-scale clear cuts through the forest have resulted in nearly no ecotones, which are essential for creating an adaptive gradient of microbes, hosts, and vectors. This may be temporarily preventing virus emergence. Nevertheless, the mid-term effect of such drastic changes in habitats and landscapes, coupled with explosive urbanization and climate changes, must not be overlooked by health authorities.
{"title":"The Risk of Virus Emergence in South America: A Subtle Balance Between Increasingly Favorable Conditions and a Protective Environment.","authors":"Benoit de Thoisy, Tiago Gräf, Daniel Santos Mansur, Adriana Delfraro, Claudia Nunes Duarte Dos Santos","doi":"10.1146/annurev-virology-100422-024648","DOIUrl":"https://doi.org/10.1146/annurev-virology-100422-024648","url":null,"abstract":"<p><p>South American ecosystems host astonishing biodiversity, with potentially great richness in viruses. However, these ecosystems have not yet been the source of any widespread, epidemic viruses. Here we explore a set of putative causes that may explain this apparent paradox. We discuss that human presence in South America is recent, beginning around 14,000 years ago; that few domestications of native species have occurred; and that successive immigration events associated with Old World virus introductions reduced the likelihood of spillovers and adaptation of local viruses into humans. Also, the diversity and ecological characteristics of vertebrate hosts might serve as protective factors. Moreover, although forest areas remained well preserved until recently, current brutal, sudden, and large-scale clear cuts through the forest have resulted in nearly no ecotones, which are essential for creating an adaptive gradient of microbes, hosts, and vectors. This may be temporarily preventing virus emergence. Nevertheless, the mid-term effect of such drastic changes in habitats and landscapes, coupled with explosive urbanization and climate changes, must not be overlooked by health authorities.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":null,"pages":null},"PeriodicalIF":11.3,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141288752","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}