Pub Date : 2024-02-27eCollection Date: 2024-01-01DOI: 10.1093/ve/veae017
Paula Lagan, Michael Hamil, Susan Cull, Anthony Hanrahan, Rosanna M Wregor, Ken Lemon
Swine influenza A virus (swIAV) is one of the main viral pathogens responsible for respiratory disease in farmed pigs. While outbreaks are often epidemic in nature, increasing reports suggest that continuous, endemic infection of herds is now common. The move towards larger herd sizes and increased intensification in the commercial pig industry may promote endemic infection; however, the impact that intensification has on swIAV infection dynamics and evolution is unclear. We carried out a longitudinal surveillance study for over 18 months on two enzootically infected, intensive, indoor, and multi-site pig production flows. Frequent sampling of all production stages using individual and group sampling methods was performed, followed by virological and immunological testing and whole-genome sequencing. We identified weaned pigs between 4 and 12-weeks old as the main reservoir of swIAV in the production flows, with continuous, year-round infection. Despite the continuous nature of viral circulation, infection levels were not uniform, with increasing exposure at the herd level associated with reduced viral prevalence followed by subsequent rebound infection. A single virus subtype was maintained on each farm for the entire duration of the study. Viral evolution was characterised by long periods of stasis punctuated by periods of rapid change coinciding with increasing exposure within the herd. An accumulation of mutations in the surface glycoproteins consistent with antigenic drift was observed, in addition to amino acid substitutions in the internal gene products as well as reassortment exchange of internal gene segments from newly introduced strains. These data demonstrate that long-term, continuous infection of herds with a single subtype is possible and document the evolutionary mechanisms utilised to achieve this.
{"title":"Swine influenza A virus infection dynamics and evolution in intensive pig production systems.","authors":"Paula Lagan, Michael Hamil, Susan Cull, Anthony Hanrahan, Rosanna M Wregor, Ken Lemon","doi":"10.1093/ve/veae017","DOIUrl":"10.1093/ve/veae017","url":null,"abstract":"<p><p>Swine influenza A virus (swIAV) is one of the main viral pathogens responsible for respiratory disease in farmed pigs. While outbreaks are often epidemic in nature, increasing reports suggest that continuous, endemic infection of herds is now common. The move towards larger herd sizes and increased intensification in the commercial pig industry may promote endemic infection; however, the impact that intensification has on swIAV infection dynamics and evolution is unclear. We carried out a longitudinal surveillance study for over 18 months on two enzootically infected, intensive, indoor, and multi-site pig production flows. Frequent sampling of all production stages using individual and group sampling methods was performed, followed by virological and immunological testing and whole-genome sequencing. We identified weaned pigs between 4 and 12-weeks old as the main reservoir of swIAV in the production flows, with continuous, year-round infection. Despite the continuous nature of viral circulation, infection levels were not uniform, with increasing exposure at the herd level associated with reduced viral prevalence followed by subsequent rebound infection. A single virus subtype was maintained on each farm for the entire duration of the study. Viral evolution was characterised by long periods of stasis punctuated by periods of rapid change coinciding with increasing exposure within the herd. An accumulation of mutations in the surface glycoproteins consistent with antigenic drift was observed, in addition to amino acid substitutions in the internal gene products as well as reassortment exchange of internal gene segments from newly introduced strains. These data demonstrate that long-term, continuous infection of herds with a single subtype is possible and document the evolutionary mechanisms utilised to achieve this.</p>","PeriodicalId":56026,"journal":{"name":"Virus Evolution","volume":"10 1","pages":"veae017"},"PeriodicalIF":5.3,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10930190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140112286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Despite a relatively low mutation rate, the large number of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections has allowed for substantial genetic change, leading to a multitude of emerging variants. Using a recently determined mutation rate (per site replication), as well as within-host parameter estimates for symptomatic SARS-CoV-2 infection, we apply a stochastic transmission-bottleneck model to describe the survival probability of de novo SARS-CoV-2 mutations as a function of bottleneck size and selection coefficient. For narrow bottlenecks, we find that mutations affecting per-target-cell attachment rate (with phenotypes associated with fusogenicity and ACE2 binding) have similar transmission probabilities to mutations affecting viral load clearance (with phenotypes associated with humoral evasion). We further find that mutations affecting the eclipse rate (with phenotypes associated with reorganization of cellular metabolic processes and synthesis of viral budding precursor material) are highly favoured relative to all other traits examined. We find that mutations leading to reduced removal rates of infected cells (with phenotypes associated with innate immune evasion) have limited transmission advantage relative to mutations leading to humoral evasion. Predicted transmission probabilities, however, for mutations affecting innate immune evasion are more consistent with the range of clinically estimated household transmission probabilities for de novo mutations. This result suggests that although mutations affecting humoral evasion are more easily transmitted when they occur, mutations affecting innate immune evasion may occur more readily. We examine our predictions in the context of a number of previously characterized mutations in circulating strains of SARS-CoV-2. Our work offers both a null model for SARS-CoV-2 mutation rates and predicts which aspects of viral life history are most likely to successfully evolve, despite low mutation rates and repeated transmission bottlenecks.
{"title":"Within-host evolution of SARS-CoV-2: how often are de novo mutations transmitted from symptomatic infections?","authors":"Chapin S Korosec, Lindi M Wahl, Jane M Heffernan","doi":"10.1093/ve/veae006","DOIUrl":"https://doi.org/10.1093/ve/veae006","url":null,"abstract":"Despite a relatively low mutation rate, the large number of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections has allowed for substantial genetic change, leading to a multitude of emerging variants. Using a recently determined mutation rate (per site replication), as well as within-host parameter estimates for symptomatic SARS-CoV-2 infection, we apply a stochastic transmission-bottleneck model to describe the survival probability of de novo SARS-CoV-2 mutations as a function of bottleneck size and selection coefficient. For narrow bottlenecks, we find that mutations affecting per-target-cell attachment rate (with phenotypes associated with fusogenicity and ACE2 binding) have similar transmission probabilities to mutations affecting viral load clearance (with phenotypes associated with humoral evasion). We further find that mutations affecting the eclipse rate (with phenotypes associated with reorganization of cellular metabolic processes and synthesis of viral budding precursor material) are highly favoured relative to all other traits examined. We find that mutations leading to reduced removal rates of infected cells (with phenotypes associated with innate immune evasion) have limited transmission advantage relative to mutations leading to humoral evasion. Predicted transmission probabilities, however, for mutations affecting innate immune evasion are more consistent with the range of clinically estimated household transmission probabilities for de novo mutations. This result suggests that although mutations affecting humoral evasion are more easily transmitted when they occur, mutations affecting innate immune evasion may occur more readily. We examine our predictions in the context of a number of previously characterized mutations in circulating strains of SARS-CoV-2. Our work offers both a null model for SARS-CoV-2 mutation rates and predicts which aspects of viral life history are most likely to successfully evolve, despite low mutation rates and repeated transmission bottlenecks.","PeriodicalId":56026,"journal":{"name":"Virus Evolution","volume":"2 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139945846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Idrissa Nonmon Sanogo, Claire Guinat, Simon Dellicour, Mohamed Adama Diakité, Mamadou Niang, Ousmane A Koita, Christelle Camus, Mariette Ducatez
Avian influenza viruses (AIV) of the H9N2 subtype have become widespread in Western Africa since their first detection in 2017 in Burkina Faso. However, the genetic characteristics and diffusion patterns of the H9N2 virus remain poorly understood in Western Africa, mainly due to limited surveillance activities. In addition, Mali, a country considered to play an important role in the epidemiology of avian influenza viruses in the region, lacks more comprehensive data on the genetic characteristics of these viruses, especially H9N2 subtype. To better understand the genetic characteristics and spatiotemporal dynamics of H9N2 virus within this region, we carried out a comprehensive genetic characterization of H9N2 viruses collected through active surveillance in live bird markets in Mali between 2021 and 2022. We also performed a continuous phylogeographic analysis to unravel the dispersal history of H9N2 lineages between Northern and Western Africa. The identified Malian H9N2 virus belonged to the G1 lineage, similar to viruses circulating in both Western and Northern Africa, and possessed multiple molecular markers associated with an increased potential for zoonotic transmission and virulence. Notably, some Malian strains carried the RSNR motif at their cleavage site, mainly observed in H9N2 strains in Asia. Our continuous phylogeographic analysis revealed a single and significant long-distance lineage dispersal event of the H9N2 virus to Western Africa, likely to have originated from Morocco in 2015, shaping the westward diffusion of the H9N2 virus. Our study highlights the need for long-term surveillance of H9N2 viruses in poultry populations in Western Africa, which is crucial for a better understanding of virus evolution and effective management against potential zoonotic AIV strain emergence.
{"title":"Genetic insights of H9N2 avian influenza viruses circulating in Mali and phylogeographic patterns in Northern and Western Africa","authors":"Idrissa Nonmon Sanogo, Claire Guinat, Simon Dellicour, Mohamed Adama Diakité, Mamadou Niang, Ousmane A Koita, Christelle Camus, Mariette Ducatez","doi":"10.1093/ve/veae011","DOIUrl":"https://doi.org/10.1093/ve/veae011","url":null,"abstract":"Avian influenza viruses (AIV) of the H9N2 subtype have become widespread in Western Africa since their first detection in 2017 in Burkina Faso. However, the genetic characteristics and diffusion patterns of the H9N2 virus remain poorly understood in Western Africa, mainly due to limited surveillance activities. In addition, Mali, a country considered to play an important role in the epidemiology of avian influenza viruses in the region, lacks more comprehensive data on the genetic characteristics of these viruses, especially H9N2 subtype. To better understand the genetic characteristics and spatiotemporal dynamics of H9N2 virus within this region, we carried out a comprehensive genetic characterization of H9N2 viruses collected through active surveillance in live bird markets in Mali between 2021 and 2022. We also performed a continuous phylogeographic analysis to unravel the dispersal history of H9N2 lineages between Northern and Western Africa. The identified Malian H9N2 virus belonged to the G1 lineage, similar to viruses circulating in both Western and Northern Africa, and possessed multiple molecular markers associated with an increased potential for zoonotic transmission and virulence. Notably, some Malian strains carried the RSNR motif at their cleavage site, mainly observed in H9N2 strains in Asia. Our continuous phylogeographic analysis revealed a single and significant long-distance lineage dispersal event of the H9N2 virus to Western Africa, likely to have originated from Morocco in 2015, shaping the westward diffusion of the H9N2 virus. Our study highlights the need for long-term surveillance of H9N2 viruses in poultry populations in Western Africa, which is crucial for a better understanding of virus evolution and effective management against potential zoonotic AIV strain emergence.","PeriodicalId":56026,"journal":{"name":"Virus Evolution","volume":"42 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139924313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
William M Switzer, Anupama Shankar, Hongwei Jia, Sergey Knyazev, Frank Ambrosio, Reagan Kelly, HaoQiang Zheng, Ellsworth M Campbell, Roxana Cintron, Yi Pan, Neeraja Saduvala, Nivedha Panneer, Rhiannon Richman, Manny B Singh, Douglas A Thoroughman, Erin F Blau, George M Khalil, Sheryl Lyss, Walid Heneine
We investigated transmission dynamics of a large HIV outbreak among persons who inject drugs (PWID) in Kentucky and Ohio during 2017–2020 by using detailed phylogenetic, network, recombination, and cluster dating analyses. Using polymerase (pol) sequences from 193 people associated with the investigation, we document high HIV-1 diversity, including subtype B (44.6 per cent); numerous circulating recombinant forms (CRFs) including CRF02_AG (2.5 per cent) and CRF02_AG-like (21.8 per cent); and many unique recombinant forms (URFs) composed of CRFs with major subtypes and sub-subtypes (CRF02_AG/B (24.3 per cent), B/CRF02_AG/B (0.5 per cent), and A6/D/B (6.4 per cent)). Cluster analysis of sequences using a 1.5 per cent genetic distance identified 13 clusters, including a 75-member cluster composed of CRF02_AG-like and CRF02_AG/B, an 18-member CRF02_AG/B cluster, subtype B clusters of sizes ranging from two to 23, and a 9-member A6/D and A6/D/B cluster. Recombination and phylogenetic analyses identified CRF02_AG/B variants with 10 unique breakpoints likely originating from subtype B and CRF02_AG-like viruses in the largest clusters. The addition of contact tracing results from Ohio to the genetic networks identified linkage between persons with subtype B, CRF02_AG, and CRF02_AG/B sequences in the clusters supporting de novo recombinant generation. Superinfection prevalence was 13.3 per cent (8/60) in persons with multiple specimens and included infection with B and CRF02_AG; B and CRF02_AG/B; or B and A6/D/B. In addition to the presence of multiple, distinct molecular clusters associated with this outbreak, cluster dating inferred transmission associated with the largest molecular cluster occurred as early as 2006, with high transmission rates during 2017–2018 in certain other molecular clusters. This outbreak among PWID in Kentucky and Ohio was likely driven by rapid transmission of multiple HIV-1 variants including de novo viral recombinants from circulating viruses within the community. Our findings documenting the high HIV-1 transmission rate and clustering through partner services and molecular clusters emphasize the importance of leveraging multiple different data sources and analyses, including those from disease intervention specialist investigations, to better understand outbreak dynamics and interrupt HIV spread.
我们通过详细的系统发生学、网络、重组和聚类年代分析，调查了 2017-2020 年期间肯塔基州和俄亥俄州注射吸毒者（PWID）中大规模 HIV 爆发的传播动态。利用与调查相关的 193 人的聚合酶（pol）序列，我们记录了 HIV-1 的高度多样性，包括 B 亚型（44.6%）；大量循环重组形式（CRF），包括 CRF02_AG（2.5%）和 CRF02_AG-like（21.8%）；以及由具有主要亚型和亚亚型（CRF02_AG/B（24.3%）、B/CRF02_AG/B（0.5%）和 A6/D/B（6.4%））的 CRF 组成的许多独特重组型（URF）。利用 1.5% 的遗传距离对序列进行聚类分析，发现了 13 个聚类，包括一个由 75 名成员组成的 CRF02_AG-like 和 CRF02_AG/B 聚类、一个由 18 名成员组成的 CRF02_AG/B 聚类、大小从 2 到 23 不等的 B 亚型聚类，以及一个由 9 名成员组成的 A6/D 和 A6/D/B 聚类。重组和系统发生学分析发现，在最大的集群中，CRF02_AG/B变体有10个独特的断裂点，可能源自B亚型和CRF02_AG样病毒。将俄亥俄州的接触追踪结果加入基因网络后，发现在支持从头重组的集群中，具有 B 亚型、CRF02_AG 和 CRF02_AG/B 序列的人之间存在联系。在有多个标本的人中，超级感染率为 13.3%（8/60），包括 B 和 CRF02_AG、B 和 CRF02_AG/B、或 B 和 A6/D/B。除了存在与此次疫情相关的多个不同分子集群外，集群测年推断与最大分子集群相关的传播早在 2006 年就已发生，2017-2018 年期间某些其他分子集群的传播率很高。肯塔基州和俄亥俄州的吸毒者疫情爆发很可能是由多种 HIV-1 变异体（包括来自社区内循环病毒的新生病毒重组体）的快速传播驱动的。我们的研究结果记录了 HIV-1 的高传播率以及通过伙伴服务和分子集群进行的集群传播，这强调了利用多种不同数据来源和分析（包括来自疾病干预专家调查的数据）来更好地了解疫情动态和阻断 HIV 传播的重要性。
{"title":"High HIV diversity, recombination, and superinfection revealed in a large outbreak among persons who inject drugs in Kentucky and Ohio, USA","authors":"William M Switzer, Anupama Shankar, Hongwei Jia, Sergey Knyazev, Frank Ambrosio, Reagan Kelly, HaoQiang Zheng, Ellsworth M Campbell, Roxana Cintron, Yi Pan, Neeraja Saduvala, Nivedha Panneer, Rhiannon Richman, Manny B Singh, Douglas A Thoroughman, Erin F Blau, George M Khalil, Sheryl Lyss, Walid Heneine","doi":"10.1093/ve/veae015","DOIUrl":"https://doi.org/10.1093/ve/veae015","url":null,"abstract":"We investigated transmission dynamics of a large HIV outbreak among persons who inject drugs (PWID) in Kentucky and Ohio during 2017–2020 by using detailed phylogenetic, network, recombination, and cluster dating analyses. Using polymerase (pol) sequences from 193 people associated with the investigation, we document high HIV-1 diversity, including subtype B (44.6 per cent); numerous circulating recombinant forms (CRFs) including CRF02_AG (2.5 per cent) and CRF02_AG-like (21.8 per cent); and many unique recombinant forms (URFs) composed of CRFs with major subtypes and sub-subtypes (CRF02_AG/B (24.3 per cent), B/CRF02_AG/B (0.5 per cent), and A6/D/B (6.4 per cent)). Cluster analysis of sequences using a 1.5 per cent genetic distance identified 13 clusters, including a 75-member cluster composed of CRF02_AG-like and CRF02_AG/B, an 18-member CRF02_AG/B cluster, subtype B clusters of sizes ranging from two to 23, and a 9-member A6/D and A6/D/B cluster. Recombination and phylogenetic analyses identified CRF02_AG/B variants with 10 unique breakpoints likely originating from subtype B and CRF02_AG-like viruses in the largest clusters. The addition of contact tracing results from Ohio to the genetic networks identified linkage between persons with subtype B, CRF02_AG, and CRF02_AG/B sequences in the clusters supporting de novo recombinant generation. Superinfection prevalence was 13.3 per cent (8/60) in persons with multiple specimens and included infection with B and CRF02_AG; B and CRF02_AG/B; or B and A6/D/B. In addition to the presence of multiple, distinct molecular clusters associated with this outbreak, cluster dating inferred transmission associated with the largest molecular cluster occurred as early as 2006, with high transmission rates during 2017–2018 in certain other molecular clusters. This outbreak among PWID in Kentucky and Ohio was likely driven by rapid transmission of multiple HIV-1 variants including de novo viral recombinants from circulating viruses within the community. Our findings documenting the high HIV-1 transmission rate and clustering through partner services and molecular clusters emphasize the importance of leveraging multiple different data sources and analyses, including those from disease intervention specialist investigations, to better understand outbreak dynamics and interrupt HIV spread.","PeriodicalId":56026,"journal":{"name":"Virus Evolution","volume":"15 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139924329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sambit K Mishra, Chase W Nelson, Bin Zhu, Maisa Pinheiro, Hyo Jung Lee, Michael Dean, Laurie Burdett, Meredith Yeager, Lisa Mirabello
High-coverage sequencing allows the study of variants occurring at low frequencies within samples, but is susceptible to false-positives caused by sequencing error. Ion Torrent has a very low single nucleotide variant (SNV) error rate and has been employed for the majority of human papillomavirus (HPV) whole genome sequences. However, benchmarking of intrahost SNVs (iSNVs) has been challenging, partly due to limitations imposed by the HPV life cycle. We address this problem by deep sequencing three replicates for each of 31 samples of HPV type 18 (HPV18). Errors, defined as iSNVs observed in only one of three replicates, are dominated by C→T (G→A) changes, independently of trinucleotide context. True iSNVs, defined as those observed in all three replicates, instead show a more diverse SNV type distribution, with particularly elevated C→T rates in CCG context (CCG→CTG; CGG→CAG) and C→A rates in ACG context (ACG→AAG; CGT→CTT). Characterization of true iSNVs allowed us to develop two methods for detecting true variants: (1) VCFgenie, a dynamic binomial filtering tool which uses each variant’s allele count and coverage instead of fixed frequency cut-offs; and (2) a machine learning binary classifier which trains eXtreme Gradient Boosting models on variant features such as quality and trinucleotide context. Each approach outperforms fixed-cut-off filtering of iSNVs, and performance is enhanced when both are used together. Our results provide improved methods for identifying true iSNVs in within-host applications across sequencing platforms, specifically using HPV18 as a case study.
{"title":"Improved detection of low-frequency within-host variants from deep sequencing: A case study with human papillomavirus","authors":"Sambit K Mishra, Chase W Nelson, Bin Zhu, Maisa Pinheiro, Hyo Jung Lee, Michael Dean, Laurie Burdett, Meredith Yeager, Lisa Mirabello","doi":"10.1093/ve/veae013","DOIUrl":"https://doi.org/10.1093/ve/veae013","url":null,"abstract":"High-coverage sequencing allows the study of variants occurring at low frequencies within samples, but is susceptible to false-positives caused by sequencing error. Ion Torrent has a very low single nucleotide variant (SNV) error rate and has been employed for the majority of human papillomavirus (HPV) whole genome sequences. However, benchmarking of intrahost SNVs (iSNVs) has been challenging, partly due to limitations imposed by the HPV life cycle. We address this problem by deep sequencing three replicates for each of 31 samples of HPV type 18 (HPV18). Errors, defined as iSNVs observed in only one of three replicates, are dominated by C→T (G→A) changes, independently of trinucleotide context. True iSNVs, defined as those observed in all three replicates, instead show a more diverse SNV type distribution, with particularly elevated C→T rates in CCG context (CCG→CTG; CGG→CAG) and C→A rates in ACG context (ACG→AAG; CGT→CTT). Characterization of true iSNVs allowed us to develop two methods for detecting true variants: (1) VCFgenie, a dynamic binomial filtering tool which uses each variant’s allele count and coverage instead of fixed frequency cut-offs; and (2) a machine learning binary classifier which trains eXtreme Gradient Boosting models on variant features such as quality and trinucleotide context. Each approach outperforms fixed-cut-off filtering of iSNVs, and performance is enhanced when both are used together. Our results provide improved methods for identifying true iSNVs in within-host applications across sequencing platforms, specifically using HPV18 as a case study.","PeriodicalId":56026,"journal":{"name":"Virus Evolution","volume":"93 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139767523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ji-Yun Kim, Sol Jeong, Da-Won Kim, Dong-Wook Lee, Dong-Hun Lee, Daehun Kim, Jung-Hoon Kwon
Clade 2.3.4.4b highly pathogenic avian influenza A (HPAI) viruses have been detected in wild birds worldwide, causing recurrent outbreaks since 2016. During the winter of 2021–2022, we detected 1 H5N8 and 43 H5N1 clade 2.3.4.4b HPAI viruses from wild birds in South Korea. Phylogenetic analysis revealed that HA gene of H5N1 viruses was divided into two genetically distinct groups (N1.G1 and N1.G2). Bayesian phylodynamic analysis demonstrated that wild birds play a vital role in viral transmission and long-term maintenance. We identified five genotypes (N1.G1.1, N1.G2, N1.G2.1, N1.G2.2, and N1.G2.2.1) having distinct gene segment constellations most probably produced by reassortments with low-pathogenic avian influenza viruses. Our results suggest that clade 2.3.4.4b persists in wild birds for a long time, causing continuous outbreaks, compared with previous clades of H5 HPAI viruses. Our study emphasizes the need for enhancing control measures in response to the changing viral epidemiology.
{"title":"Genomic Epidemiology of Highly Pathogenic Avian Influenza A (H5N1) Virus in Wild Birds in South Korea during 2021–2022: Changes in Viral Epidemic Patterns","authors":"Ji-Yun Kim, Sol Jeong, Da-Won Kim, Dong-Wook Lee, Dong-Hun Lee, Daehun Kim, Jung-Hoon Kwon","doi":"10.1093/ve/veae014","DOIUrl":"https://doi.org/10.1093/ve/veae014","url":null,"abstract":"Clade 2.3.4.4b highly pathogenic avian influenza A (HPAI) viruses have been detected in wild birds worldwide, causing recurrent outbreaks since 2016. During the winter of 2021–2022, we detected 1 H5N8 and 43 H5N1 clade 2.3.4.4b HPAI viruses from wild birds in South Korea. Phylogenetic analysis revealed that HA gene of H5N1 viruses was divided into two genetically distinct groups (N1.G1 and N1.G2). Bayesian phylodynamic analysis demonstrated that wild birds play a vital role in viral transmission and long-term maintenance. We identified five genotypes (N1.G1.1, N1.G2, N1.G2.1, N1.G2.2, and N1.G2.2.1) having distinct gene segment constellations most probably produced by reassortments with low-pathogenic avian influenza viruses. Our results suggest that clade 2.3.4.4b persists in wild birds for a long time, causing continuous outbreaks, compared with previous clades of H5 HPAI viruses. Our study emphasizes the need for enhancing control measures in response to the changing viral epidemiology.","PeriodicalId":56026,"journal":{"name":"Virus Evolution","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139768118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhiyong Wu, Tong Chang, Decheng Wang, Hongliang Zhang, Haizhou Liu, Xinyi Huang, Zhijun Tian, Xiaoxiao Tian, Di Liu, Tongqing An, Yi Yan
Porcine reproductive and respiratory syndrome virus (PRRSV) poses a serious threat to the pig industry in China. Our previous study demonstrated that PRRSV persists with local circulations and overseas imports in China, and has formed a relatively stable epidemic pattern. However, the sudden African swine fever (ASF) outbreak in 2018 caused serious damage to China’s pig industry structure, which resulted in about 40% of pigs being slaughtered. The pig yields recovered by the end of 2019. Thus, whether the ASF outbreak reframed PRRSV evolution with changes in pig populations, and further posed new threats to the pig industry becomes a matter of concern. For this purpose, we conducted genomic surveillance and recombination, NSP2 polymorphism, population dynamics, and geographical spread analysis of PRRSV-2, which is dominant in China. Results showed that the prevalence of ASF had no significant effects on genetic diversities like lineage composition, recombination patterns, and NSP2 insertion and deletion patterns, but was likely to lead to changes in PRRSV-2 recombination frequency. As for circulation of the two major sub-lineages of lineage 1, there was no apparent transmission of NADC30-like among provinces, while NADC34-like had obvious signs of inter-provincial transmission and foreign importation during the ASF epidemic. In addition, two suspected vaccine recombinant epidemic strains suggest a slight safety issue of vaccine use. Herein, the interference of ASF to the PRRSV-2 evolutionary pattern was evaluated and vaccine safety was analyzed, in order to monitor the potential threat of PRRSV-2 to China’s pig industry in the post-epidemic era of ASF.
{"title":"Genomic Surveillance and Evolutionary Dynamics of Type-2 Porcine Reproductive and Respiratory Syndrome Virus in China Spanning the African Swine Fever Outbreak","authors":"Zhiyong Wu, Tong Chang, Decheng Wang, Hongliang Zhang, Haizhou Liu, Xinyi Huang, Zhijun Tian, Xiaoxiao Tian, Di Liu, Tongqing An, Yi Yan","doi":"10.1093/ve/veae016","DOIUrl":"https://doi.org/10.1093/ve/veae016","url":null,"abstract":"Porcine reproductive and respiratory syndrome virus (PRRSV) poses a serious threat to the pig industry in China. Our previous study demonstrated that PRRSV persists with local circulations and overseas imports in China, and has formed a relatively stable epidemic pattern. However, the sudden African swine fever (ASF) outbreak in 2018 caused serious damage to China’s pig industry structure, which resulted in about 40% of pigs being slaughtered. The pig yields recovered by the end of 2019. Thus, whether the ASF outbreak reframed PRRSV evolution with changes in pig populations, and further posed new threats to the pig industry becomes a matter of concern. For this purpose, we conducted genomic surveillance and recombination, NSP2 polymorphism, population dynamics, and geographical spread analysis of PRRSV-2, which is dominant in China. Results showed that the prevalence of ASF had no significant effects on genetic diversities like lineage composition, recombination patterns, and NSP2 insertion and deletion patterns, but was likely to lead to changes in PRRSV-2 recombination frequency. As for circulation of the two major sub-lineages of lineage 1, there was no apparent transmission of NADC30-like among provinces, while NADC34-like had obvious signs of inter-provincial transmission and foreign importation during the ASF epidemic. In addition, two suspected vaccine recombinant epidemic strains suggest a slight safety issue of vaccine use. Herein, the interference of ASF to the PRRSV-2 evolutionary pattern was evaluated and vaccine safety was analyzed, in order to monitor the potential threat of PRRSV-2 to China’s pig industry in the post-epidemic era of ASF.","PeriodicalId":56026,"journal":{"name":"Virus Evolution","volume":"20 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139767519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Single-stranded DNA multipartite viruses, which mostly consist of members of the genus Begomovirus, family Geminiviridae and all members of the family Nanoviridae, partly resolve the cost of genomic integrity maintenance through two remarkable capacities. They are able to systemically infect a host even when their genomic segments are not together in the same host cell, and these segments can be separately transmitted by insect vectors from host to host. These capacities potentially allow such viruses to reassort at a much larger spatial scale, since reassortants could arise from parental genotypes that do not co-infect the same cell or even the same host. To assess the limitations affecting reassortment and their implications in genome integrity maintenance, the objective of this review is to identify putative molecular constraints influencing reassorted segments throughout the infection cycle, and to confront expectations based on these constraints with empirical observations. Trans-replication of the reassorted segments emerges as the major constraint, while encapsidation, viral movement, and transmission compatibilities appear more permissive. Confronting the available molecular data and the resulting predictions on reassortments to field population surveys reveals notable discrepancies, particularly a surprising rarity of inter-specific natural reassortments within the Nanoviridae family. These apparent discrepancies unveil important knowledge gaps in the biology of ssDNA multipartite viruses and call for further investigation on the role of reassortment in their biology.
单链 DNA 多组分病毒主要包括 Begomovirus 属、Geminiviridae 科和 Nanoviridae 科的所有成员，它们通过两种非凡的能力部分地解决了基因组完整性的维护成本问题。即使基因组片段不在同一个宿主细胞中，它们也能系统地感染宿主，而且这些片段可以通过昆虫载体在宿主之间单独传播。这些能力有可能使这类病毒在更大的空间范围内进行重配，因为重配子可能来自不共同感染同一细胞甚至同一宿主的亲代基因型。为了评估影响重配的限制因素及其对基因组完整性维护的影响，本综述旨在确定在整个感染周期中影响重配片段的假定分子限制因素，并将基于这些限制因素的预期与经验观察对立起来。重配片段的转录复制是主要的制约因素，而包囊化、病毒移动和传播兼容性似乎更为宽松。将现有的分子数据和由此得出的重配预测与实地种群调查相比较，会发现明显的差异，特别是纳诺病毒科内种间自然重配的罕见程度令人惊讶。这些明显的差异揭示了 ssDNA 多部分病毒生物学中的重要知识空白，并要求进一步研究重配在其生物学中的作用。
{"title":"Reassortments in Single-Stranded DNA Multipartite Viruses: Confronting Expectations Based on Molecular Constraints with Field Observations","authors":"Babil Torralba, Stéphane Blanc, Yannis Michalakis","doi":"10.1093/ve/veae010","DOIUrl":"https://doi.org/10.1093/ve/veae010","url":null,"abstract":"Single-stranded DNA multipartite viruses, which mostly consist of members of the genus Begomovirus, family Geminiviridae and all members of the family Nanoviridae, partly resolve the cost of genomic integrity maintenance through two remarkable capacities. They are able to systemically infect a host even when their genomic segments are not together in the same host cell, and these segments can be separately transmitted by insect vectors from host to host. These capacities potentially allow such viruses to reassort at a much larger spatial scale, since reassortants could arise from parental genotypes that do not co-infect the same cell or even the same host. To assess the limitations affecting reassortment and their implications in genome integrity maintenance, the objective of this review is to identify putative molecular constraints influencing reassorted segments throughout the infection cycle, and to confront expectations based on these constraints with empirical observations. Trans-replication of the reassorted segments emerges as the major constraint, while encapsidation, viral movement, and transmission compatibilities appear more permissive. Confronting the available molecular data and the resulting predictions on reassortments to field population surveys reveals notable discrepancies, particularly a surprising rarity of inter-specific natural reassortments within the Nanoviridae family. These apparent discrepancies unveil important knowledge gaps in the biology of ssDNA multipartite viruses and call for further investigation on the role of reassortment in their biology.","PeriodicalId":56026,"journal":{"name":"Virus Evolution","volume":"37 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139678646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Barney I Potter, Marijn Thijssen, Nídia Sequeira Trovão, Andrea Pineda-Peña, Marijke Reynders, Thomas Mina, Carolina Alvarez, Samad Amini-Bavil-Olyaee, Frederik Nevens, Piet Maes, Philippe Lemey, Marc Van Ranst, Guy Baele, Mahmoud Reza Pourkarim
Infection by hepatitis B virus (HBV) is responsible for approximately 296 million chronic cases of hepatitis B, and roughly 880,000 deaths annually. The global burden of HBV is distributed unevenly, largely owing to the heterogeneous geographic distribution of its subtypes, each of which demonstrates different severity and responsiveness to antiviral therapy. It is therefore crucial to the global public health response to HBV that the spatiotemporal spread of each genotype is well characterized. In this study, we describe a collection of 133 newly-sequenced HBV strains from recent African immigrants upon their arrival in Belgium. We incorporate these sequences – all of which we determine to come from genotypes A, D, and E – into a large-scale phylogeographic study with genomes sampled across the globe. We focus on investigating the spatio-temporal processes shaping the evolutionary history of the three genotypes we observe. We incorporate several recently published ancient HBV genomes for genotypes A and D to aid our analysis. We show that different spatio-temporal processes underlie the A, D and E genotypes with the former two having originated in southeastern Asia, after which they spread across the world. The HBV E genotype is estimated to have originated in Africa, after which it spread to Europe and the Americas. Our results highlight the use of phylogeographic reconstruction as a tool to understand the recent spatiotemporal dynamics of HBV, and highlight the importance of supporting vulnerable populations in accordance with the needs presented by specific HBV genotypes.
乙型肝炎病毒（HBV）感染导致每年约 2.96 亿例慢性乙型肝炎病例和约 88 万人死亡。乙型肝炎病毒造成的全球负担分布不均，这主要是由于乙型肝炎病毒亚型的地理分布不均，每种亚型的严重程度和对抗病毒治疗的反应性各不相同。因此，充分描述每种基因型的时空分布对全球应对 HBV 的公共卫生至关重要。在本研究中，我们描述了从新近抵达比利时的非洲移民中收集到的 133 个新测序的 HBV 株系。我们将这些序列--我们确定它们全部来自基因型 A、D 和 E--纳入了一项大规模的系统地理学研究，其基因组样本遍布全球。我们重点研究了影响我们观察到的三种基因型进化史的时空过程。我们纳入了最近发表的几个基因型 A 和 D 的古代 HBV 基因组，以帮助我们进行分析。我们的研究表明，A、D 和 E 基因型起源于不同的时空过程，前两种基因型起源于亚洲东南部，之后传播到世界各地。据估计，HBV E 基因型起源于非洲，之后传播到欧洲和美洲。我们的研究结果突出了利用系统地理学重建作为了解 HBV 近期时空动态的工具，并强调了根据特定 HBV 基因型提出的需求支持易感人群的重要性。
{"title":"Contemporary and historical human migration patterns shape hepatitis B virus diversity","authors":"Barney I Potter, Marijn Thijssen, Nídia Sequeira Trovão, Andrea Pineda-Peña, Marijke Reynders, Thomas Mina, Carolina Alvarez, Samad Amini-Bavil-Olyaee, Frederik Nevens, Piet Maes, Philippe Lemey, Marc Van Ranst, Guy Baele, Mahmoud Reza Pourkarim","doi":"10.1093/ve/veae009","DOIUrl":"https://doi.org/10.1093/ve/veae009","url":null,"abstract":"Infection by hepatitis B virus (HBV) is responsible for approximately 296 million chronic cases of hepatitis B, and roughly 880,000 deaths annually. The global burden of HBV is distributed unevenly, largely owing to the heterogeneous geographic distribution of its subtypes, each of which demonstrates different severity and responsiveness to antiviral therapy. It is therefore crucial to the global public health response to HBV that the spatiotemporal spread of each genotype is well characterized. In this study, we describe a collection of 133 newly-sequenced HBV strains from recent African immigrants upon their arrival in Belgium. We incorporate these sequences – all of which we determine to come from genotypes A, D, and E – into a large-scale phylogeographic study with genomes sampled across the globe. We focus on investigating the spatio-temporal processes shaping the evolutionary history of the three genotypes we observe. We incorporate several recently published ancient HBV genomes for genotypes A and D to aid our analysis. We show that different spatio-temporal processes underlie the A, D and E genotypes with the former two having originated in southeastern Asia, after which they spread across the world. The HBV E genotype is estimated to have originated in Africa, after which it spread to Europe and the Americas. Our results highlight the use of phylogeographic reconstruction as a tool to understand the recent spatiotemporal dynamics of HBV, and highlight the importance of supporting vulnerable populations in accordance with the needs presented by specific HBV genotypes.","PeriodicalId":56026,"journal":{"name":"Virus Evolution","volume":"296 1 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139662564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-27eCollection Date: 2024-01-01DOI: 10.1093/ve/veae005
Bin Ma, Huimin Gong, Qianshuai Xu, Yuan Gao, Aohan Guan, Haoyu Wang, Kexin Hua, Rui Luo, Hui Jin
Understanding phylogenetic relationships among species is essential for many biological studies, which call for an accurate phylogenetic tree to understand major evolutionary transitions. The phylogenetic analyses present a major challenge in estimation accuracy and computational efficiency, especially recently facing a wave of severe emerging infectious disease outbreaks. Here, we introduced a novel, efficient framework called Bases-dependent Rapid Phylogenetic Clustering (Bd-RPC) for new sample placement for viruses. In this study, a brand-new recoding method called Frequency Vector Recoding was implemented to approximate the phylogenetic distance, and the Phylogenetic Simulated Annealing Search algorithm was developed to match the recoded distance matrix with the phylogenetic tree. Meanwhile, the indel (insertion/deletion) was heuristically introduced to foreign sequence recognition for the first time. Here, we compared the Bd-RPC with the recent placement software (PAGAN2, EPA-ng, TreeBeST) and evaluated it in Alphacoronavirus, Alphaherpesvirinae, and Betacoronavirus by using Split and Robinson-Foulds distances. The comparisons showed that Bd-RPC maintained the highest precision with great efficiency, demonstrating good performance in new sample placement on all three virus genera. Finally, a user-friendly website (http://www.bd-rpc.xyz) is available for users to classify new samples instantly and facilitate exploration of the phylogenetic research in viruses, and the Bd-RPC is available on GitHub (http://github.com/Bin-Ma/bd-rpc).
{"title":"Bases-dependent Rapid Phylogenetic Clustering (Bd-RPC) enables precise and efficient phylogenetic estimation in viruses.","authors":"Bin Ma, Huimin Gong, Qianshuai Xu, Yuan Gao, Aohan Guan, Haoyu Wang, Kexin Hua, Rui Luo, Hui Jin","doi":"10.1093/ve/veae005","DOIUrl":"10.1093/ve/veae005","url":null,"abstract":"<p><p>Understanding phylogenetic relationships among species is essential for many biological studies, which call for an accurate phylogenetic tree to understand major evolutionary transitions. The phylogenetic analyses present a major challenge in estimation accuracy and computational efficiency, especially recently facing a wave of severe emerging infectious disease outbreaks. Here, we introduced a novel, efficient framework called Bases-dependent Rapid Phylogenetic Clustering (Bd-RPC) for new sample placement for viruses. In this study, a brand-new recoding method called Frequency Vector Recoding was implemented to approximate the phylogenetic distance, and the Phylogenetic Simulated Annealing Search algorithm was developed to match the recoded distance matrix with the phylogenetic tree. Meanwhile, the indel (insertion/deletion) was heuristically introduced to foreign sequence recognition for the first time. Here, we compared the Bd-RPC with the recent placement software (PAGAN2, EPA-ng, TreeBeST) and evaluated it in <i>Alphacoronavirus, Alphaherpesvirinae</i>, and <i>Betacoronavirus</i> by using Split and Robinson-Foulds distances. The comparisons showed that Bd-RPC maintained the highest precision with great efficiency, demonstrating good performance in new sample placement on all three virus genera. Finally, a user-friendly website (http://www.bd-rpc.xyz) is available for users to classify new samples instantly and facilitate exploration of the phylogenetic research in viruses, and the Bd-RPC is available on GitHub (http://github.com/Bin-Ma/bd-rpc).</p>","PeriodicalId":56026,"journal":{"name":"Virus Evolution","volume":"10 1","pages":"veae005"},"PeriodicalIF":5.3,"publicationDate":"2024-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10868571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139742786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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