Pub Date : 2025-06-01Epub Date: 2024-11-12DOI: 10.1080/03079457.2024.2423716
Xin Yi, Huabin Cao, Jianzhao Liao, Wenlan Yu, Guoliang Hu, Zhaoxin Tang, Fan Yang
Copper (Cu) is a necessary micro-element and plays important roles in many biochemical processes. However, excessive Cu intake can lead to multi-organ toxicity, especially in the spleen. To gain further insights into the specific mechanisms of splenic toxicity associated with Cu-induced metabolic disorders, 192 one-day-old chickens were selected and randomly divided into four groups for this study. The broilers were fed with diets containing Cu at final concentrations of 11, 110, 220 and 330 mg/kg for 49 days. The results showed that high dietary Cu caused nuclear shrinkage and mitochondrial vacuolization in the spleen and induced splenic injury through regulating the glutathione metabolism, pentose and gluconate interconversion, tryptophan metabolism and glycerophosphatidylcholine metabolism pathways. Moreover, excess Cu could disorder the mitochondrial dynamics via up-regulating the levels of Drp1, Parkin PINK1, and Dynein, and down-regulating the levels of Mfn1, Mfn2 and OPA1. Cu treatment increased the levels of LC3A, LC3B, mTOR, Beclin1, and ATG5 and decreased the p62 level to promote autophagy of splenocytes. Meanwhile, a high dose of Cu promoted splenocyte apoptosis by increasing the levels of p53, BAK-1, Bax, Cyt C and Caspase-3 and decreasing the level of Bcl-2. These results demonstrated that high dietary Cu could cause autophagy and apoptosis via inducing metabolic disturbances and disordering mitochondrial dynamics in the spleen of broiler chicken.
{"title":"Metabolomics analysis reveals the effects of high dietary copper on mitochondria-mediated autophagy and apoptosis in spleen of broiler chicken.","authors":"Xin Yi, Huabin Cao, Jianzhao Liao, Wenlan Yu, Guoliang Hu, Zhaoxin Tang, Fan Yang","doi":"10.1080/03079457.2024.2423716","DOIUrl":"10.1080/03079457.2024.2423716","url":null,"abstract":"<p><p>Copper (Cu) is a necessary micro-element and plays important roles in many biochemical processes. However, excessive Cu intake can lead to multi-organ toxicity, especially in the spleen. To gain further insights into the specific mechanisms of splenic toxicity associated with Cu-induced metabolic disorders, 192 one-day-old chickens were selected and randomly divided into four groups for this study. The broilers were fed with diets containing Cu at final concentrations of 11, 110, 220 and 330 mg/kg for 49 days. The results showed that high dietary Cu caused nuclear shrinkage and mitochondrial vacuolization in the spleen and induced splenic injury through regulating the glutathione metabolism, pentose and gluconate interconversion, tryptophan metabolism and glycerophosphatidylcholine metabolism pathways. Moreover, excess Cu could disorder the mitochondrial dynamics via up-regulating the levels of Drp1, Parkin PINK1, and Dynein, and down-regulating the levels of Mfn1, Mfn2 and OPA1. Cu treatment increased the levels of LC3A, LC3B, mTOR, Beclin1, and ATG5 and decreased the p62 level to promote autophagy of splenocytes. Meanwhile, a high dose of Cu promoted splenocyte apoptosis by increasing the levels of p53, BAK-1, Bax, Cyt C and Caspase-3 and decreasing the level of Bcl-2. These results demonstrated that high dietary Cu could cause autophagy and apoptosis via inducing metabolic disturbances and disordering mitochondrial dynamics in the spleen of broiler chicken.</p>","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"306-316"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2024-12-17DOI: 10.1080/03079457.2024.2425353
Yi Tang, Haiyang Yu, Muhammad Zubair Shabbir, Carrington Stephenson, Patrica A Dunn, Eva A Wallner-Pendleton, Huaguang Lu
ABSTRACTWe conducted research studies on avian reovirus (ARV) infectivity in egg-laying hens, focusing on three variants (δC genotypes 2, 3, and 5) detected in layer chickens in Pennsylvania to date. Day-old chicks (Hy-Line North America, LLC, PA), raised at the Poultry Education and Research Center of Penn State University Park campus, showed healthy growth and normal egg production after 20 weeks of age. ARV variants were propagated in Leghorn male-chicken hepatocellular-carcinoma cell cultures, with concentrations measured at TCID50/ml. Each group of 10 hens received a 1.0 ml dose containing 103-104 TCID50/ml of one ARV variant through oral, nasal, and ocular routes. Infected hens showed normal egg production, with minimal signs of watery droppings in the first-week post-inoculation (pi). Cloacal and oral pharyngeal swabs were collected daily in the first week pi and every other day in the second-week pi to monitor virus shedding. Virus shedding began 24 h pi through faeces, peaked at 2-4 days pi, decreased by 5-7 days pi, and ceased after 12-14 days pi. A few birds' oral pharyngeal swabs were weakly positive for 1-3 days pi, then all turned negative. Infected hens developed high serum and egg yolk antibody titres at 2-3 weeks pi, showing 100% protection against subsequent infections with the same variant strain, demonstrating a 100% protection rate.RESEARCH HIGHLIGHTSAvian reovirus-infected hens shed virus heavily at 2-3 days post-inoculation.Shedding became minimal after 5-7 days post-inoculation.ARV variants offered 100% protection in hens upon subsequent infections.Infected hens maintained normal egg production with no observable clinical signs.
{"title":"Evaluation of infectivity, length of infection, and immune response of avian reovirus variants in egg-laying hens.","authors":"Yi Tang, Haiyang Yu, Muhammad Zubair Shabbir, Carrington Stephenson, Patrica A Dunn, Eva A Wallner-Pendleton, Huaguang Lu","doi":"10.1080/03079457.2024.2425353","DOIUrl":"10.1080/03079457.2024.2425353","url":null,"abstract":"<p><p><b>ABSTRACT</b>We conducted research studies on avian reovirus (ARV) infectivity in egg-laying hens, focusing on three variants (δC genotypes 2, 3, and 5) detected in layer chickens in Pennsylvania to date. Day-old chicks (Hy-Line North America, LLC, PA), raised at the Poultry Education and Research Center of Penn State University Park campus, showed healthy growth and normal egg production after 20 weeks of age. ARV variants were propagated in Leghorn male-chicken hepatocellular-carcinoma cell cultures, with concentrations measured at TCID<sub>50</sub>/ml. Each group of 10 hens received a 1.0 ml dose containing 10<sup>3</sup>-10<sup>4</sup> TCID<sub>50</sub>/ml of one ARV variant through oral, nasal, and ocular routes. Infected hens showed normal egg production, with minimal signs of watery droppings in the first-week post-inoculation (pi). Cloacal and oral pharyngeal swabs were collected daily in the first week pi and every other day in the second-week pi to monitor virus shedding. Virus shedding began 24 h pi through faeces, peaked at 2-4 days pi, decreased by 5-7 days pi, and ceased after 12-14 days pi. A few birds' oral pharyngeal swabs were weakly positive for 1-3 days pi, then all turned negative. Infected hens developed high serum and egg yolk antibody titres at 2-3 weeks pi, showing 100% protection against subsequent infections with the same variant strain, demonstrating a 100% protection rate.<b>RESEARCH HIGHLIGHTS</b>Avian reovirus-infected hens shed virus heavily at 2-3 days post-inoculation.Shedding became minimal after 5-7 days post-inoculation.ARV variants offered 100% protection in hens upon subsequent infections.Infected hens maintained normal egg production with no observable clinical signs.</p>","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"317-324"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-01-13DOI: 10.1080/03079457.2024.2442704
Lumin Yu, Hui Wang, Xinglin Zhang, Ting Xue
Avian pathogenic Escherichia coli (APEC) is an important zoonotic pathogen that infects avian species by colonizing the gastrointestinal, respiratory, or reproductive tracts, leading to significant economic losses to the poultry industry worldwide and threatening food security and human health. APEC has evolved the two-component signal transduction system (TCS) to adapt and respond to extracellular environmental stresses, which are produced when the host is invaded by APEC. Here, we focus on the effect of the UhpAB TCS on the pathogenicity of APEC. The results in this study showed that the UhpAB TCS contributed to the pathogenicity of APEC in a chicken infection model. The electrophoretic mobility shift assays (EMSA) confirmed that UhpAB specifically bound to the promoters of fepG, ldrD, ycgV, and ydeI, and activated their expression, measured using real-time reverse transcription PCR (real-time RT-PCR). Furthermore, the UhpAB TCS could promote biofilm formation by activating the expression of biofilm master transcriptional regulator encoding gene csgD and enhance stress tolerance by activating the expression of stress protein encoding genes uspA and bhsA, thereby assisting APEC to evade host immune responses and inflammatory responses, and increasing the pathogenicity of APEC. These findings deepen our understanding of the pathogenic mechanism in APEC and offer new perspectives for further studies on the prevention and control of APEC infection.RESEARCH HIGHLIGHTSUhpAB increases the pathogenicity of APEC.UhpAB activates the expression of virulence genes fepG, ldrD, ycgV, and ydeI.UhpAB promotes biofilm formation and enhances stress tolerance.UhpAB contributes to APEC evading attack by the host immune system.
{"title":"Two-component system UhpAB facilitates the pathogenicity of avian pathogenic <i>Escherichia coli</i> through biofilm formation and stress responses.","authors":"Lumin Yu, Hui Wang, Xinglin Zhang, Ting Xue","doi":"10.1080/03079457.2024.2442704","DOIUrl":"10.1080/03079457.2024.2442704","url":null,"abstract":"<p><p>Avian pathogenic <i>Escherichia coli</i> (APEC) is an important zoonotic pathogen that infects avian species by colonizing the gastrointestinal, respiratory, or reproductive tracts, leading to significant economic losses to the poultry industry worldwide and threatening food security and human health. APEC has evolved the two-component signal transduction system (TCS) to adapt and respond to extracellular environmental stresses, which are produced when the host is invaded by APEC. Here, we focus on the effect of the UhpAB TCS on the pathogenicity of APEC. The results in this study showed that the UhpAB TCS contributed to the pathogenicity of APEC in a chicken infection model. The electrophoretic mobility shift assays (EMSA) confirmed that UhpAB specifically bound to the promoters of <i>fepG</i>, <i>ldrD</i>, <i>ycgV</i>, and <i>ydeI</i>, and activated their expression, measured using real-time reverse transcription PCR (real-time RT-PCR). Furthermore, the UhpAB TCS could promote biofilm formation by activating the expression of biofilm master transcriptional regulator encoding gene <i>csgD</i> and enhance stress tolerance by activating the expression of stress protein encoding genes <i>uspA</i> and <i>bhsA</i>, thereby assisting APEC to evade host immune responses and inflammatory responses, and increasing the pathogenicity of APEC. These findings deepen our understanding of the pathogenic mechanism in APEC and offer new perspectives for further studies on the prevention and control of APEC infection.<b>RESEARCH HIGHLIGHTS</b>UhpAB increases the pathogenicity of APEC.UhpAB activates the expression of virulence genes <i>fepG</i>, <i>ldrD</i>, <i>ycgV</i>, and <i>ydeI</i>.UhpAB promotes biofilm formation and enhances stress tolerance.UhpAB contributes to APEC evading attack by the host immune system.</p>","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"359-370"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-01-02DOI: 10.1080/03079457.2024.2441180
Damer P Blake
ABSTRACTEimeria are globally enzootic parasites that can cause coccidiosis in chickens. Until recently, remarkably little had changed over the last 40 years in the fundamental biology that underpins detection and control of Eimeria. Tools such as microscopy and lesion scoring remain central to diagnosis, and control still relies on routine supplementation of diets with anticoccidial drugs or application of live vaccines. However, refocusing on aspects of economics, molecular biology, and bacteriology that relate to coccidiosis has prompted considerable change in dogma. The cost of coccidiosis in chickens has been difficult to define, but updating models created in the 1990s suggested an annual cost to the global poultry industry of £10.4 billion in 2016, rising to a peak of £12.9 billion in 2022 under the influence of the COVID-19 pandemic and regional wars. Surveillance using genomic sequence-based diagnostics has suggested the presence of three new Eimeria species, supported by subsequent biological characterization of each line. Use of microbiome sequencing pipelines has revealed the breadth of impact Eimeria infection exerts on enteric microbiota, contributing to dysbiosis and deteriorating litter conditions. Enhanced understanding of Eimeria and the consequences of infection can be used to improve control and diagnosis with relevance to productivity and welfare, creating opportunities to optimize anticoccidial drug use.RESEARCH HIGHLIGHTSThe cost of coccidiosis in chickens fluctuates considerably, peaking in 2022.Three new Eimeria species can infect chickens and escape current vaccines.Eimeria infection exerts wide-ranging effects on enteric microbiota.
{"title":"<i>Eimeria</i> of chickens: the changing face of an old foe.","authors":"Damer P Blake","doi":"10.1080/03079457.2024.2441180","DOIUrl":"10.1080/03079457.2024.2441180","url":null,"abstract":"<p><p><b>ABSTRACT</b><i>Eimeria</i> are globally enzootic parasites that can cause coccidiosis in chickens. Until recently, remarkably little had changed over the last 40 years in the fundamental biology that underpins detection and control of <i>Eimeria</i>. Tools such as microscopy and lesion scoring remain central to diagnosis, and control still relies on routine supplementation of diets with anticoccidial drugs or application of live vaccines. However, refocusing on aspects of economics, molecular biology, and bacteriology that relate to coccidiosis has prompted considerable change in dogma. The cost of coccidiosis in chickens has been difficult to define, but updating models created in the 1990s suggested an annual cost to the global poultry industry of £10.4 billion in 2016, rising to a peak of £12.9 billion in 2022 under the influence of the COVID-19 pandemic and regional wars. Surveillance using genomic sequence-based diagnostics has suggested the presence of three new <i>Eimeria</i> species, supported by subsequent biological characterization of each line. Use of microbiome sequencing pipelines has revealed the breadth of impact <i>Eimeria</i> infection exerts on enteric microbiota, contributing to dysbiosis and deteriorating litter conditions. Enhanced understanding of <i>Eimeria</i> and the consequences of infection can be used to improve control and diagnosis with relevance to productivity and welfare, creating opportunities to optimize anticoccidial drug use.<b>RESEARCH HIGHLIGHTS</b>The cost of coccidiosis in chickens fluctuates considerably, peaking in 2022.Three new <i>Eimeria</i> species can infect chickens and escape current vaccines.<i>Eimeria</i> infection exerts wide-ranging effects on enteric microbiota.</p>","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"267-278"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142913796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-01-03DOI: 10.1080/03079457.2024.2441175
Caterina Lupini, Nicla Gentile, Giulia Graziosi, Giulia Quaglia, Gabriele Lizzi, Sara Pedrazzoli, Claudia M Tucciarone, Giovanni Franzo, Matteo Legnardi, Riccardo Baston, Mattia Cecchinato, Laura Menotti, Renato Brandimarti, Elisa Avitabile, Elena Catelli
Avian metapneumovirus (aMPV) is an important pathogen in poultry, primarily affecting chickens and turkeys, and it causes acute respiratory disease or reproductive disorders. Considering previous molecular or serological evidence of aMPV in different wild bird species, the role of non-domestic hosts in the virus epidemiology has been called into question. A molecular survey was therefore performed on wild aquatic bird species sampled during the Italian Avian Influenza Surveillance plan from 2021-2023 in the Bologna province. A total of 250 oropharyngeal swabs were collected and screened for all circulating aMPV subtypes through multiplex real-time RT-PCR. An aMPV-B strain, named aMPV/B/Italy/Northern_shoveler/80/21, was detected in an adult Northern shoveler (Spatula clypeata) wintering in Italy in 2021, and it was characterized by partial amplification and sequencing of the attachment glycoprotein gene. Phylogenetic analysis showed close relationships between this strain and those circulating in Italian poultry from 2014-2019. Given the high aMPV-B burden on the Italian poultry sector and the similarity of aMPV/B/Italy/Northern_shoveler/80/21 strain to those circulating in chickens and turkeys, potential virus spillover from domestic to wild birds could have occurred at the livestock-wildlife interface. Considering that aMPV-B is well adapted to gallinaceans, this represents one of the rare molecular detections of this subtype in waterfowl species. Expanding aMPV monitoring and conducting further biological studies on wild hosts are essential for a better understanding of their role in maintaining aMPV circulation.RESEARCH HIGHLIGHTSWild birds sampled in Italy tested for aMPV detection and characterization.aMPV-B found for the first time in a wintering Northern shoveler.Close phylogenetic relationship with aMPV-B strains circulating in Italian poultry.
{"title":"Avian metapneumovirus subtype B in a Northern shoveler (<i>Spatula clypeata</i>) wintering in Italy: implications for the domestic-wild bird interface?","authors":"Caterina Lupini, Nicla Gentile, Giulia Graziosi, Giulia Quaglia, Gabriele Lizzi, Sara Pedrazzoli, Claudia M Tucciarone, Giovanni Franzo, Matteo Legnardi, Riccardo Baston, Mattia Cecchinato, Laura Menotti, Renato Brandimarti, Elisa Avitabile, Elena Catelli","doi":"10.1080/03079457.2024.2441175","DOIUrl":"10.1080/03079457.2024.2441175","url":null,"abstract":"<p><p>Avian metapneumovirus (aMPV) is an important pathogen in poultry, primarily affecting chickens and turkeys, and it causes acute respiratory disease or reproductive disorders. Considering previous molecular or serological evidence of aMPV in different wild bird species, the role of non-domestic hosts in the virus epidemiology has been called into question. A molecular survey was therefore performed on wild aquatic bird species sampled during the Italian Avian Influenza Surveillance plan from 2021-2023 in the Bologna province. A total of 250 oropharyngeal swabs were collected and screened for all circulating aMPV subtypes through multiplex real-time RT-PCR. An aMPV-B strain, named aMPV/B/Italy/Northern_shoveler/80/21, was detected in an adult Northern shoveler (<i>Spatula clypeata</i>) wintering in Italy in 2021, and it was characterized by partial amplification and sequencing of the attachment glycoprotein gene. Phylogenetic analysis showed close relationships between this strain and those circulating in Italian poultry from 2014-2019. Given the high aMPV-B burden on the Italian poultry sector and the similarity of aMPV/B/Italy/Northern_shoveler/80/21 strain to those circulating in chickens and turkeys, potential virus spillover from domestic to wild birds could have occurred at the livestock-wildlife interface. Considering that aMPV-B is well adapted to gallinaceans, this represents one of the rare molecular detections of this subtype in waterfowl species. Expanding aMPV monitoring and conducting further biological studies on wild hosts are essential for a better understanding of their role in maintaining aMPV circulation.<b>RESEARCH HIGHLIGHTS</b>Wild birds sampled in Italy tested for aMPV detection and characterization.aMPV-B found for the first time in a wintering Northern shoveler.Close phylogenetic relationship with aMPV-B strains circulating in Italian poultry.</p>","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"351-358"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2024-11-18DOI: 10.1080/03079457.2024.2420712
Sungsu Youk, Dong-Hun Lee, David E Swayne, Mary Lea Killian, Mia Kim Torchetti
The H2N2 avian influenza viruses (AIV) have been reported in the Northeast United States of America (USA) live bird market (LBM) system since 2014. In this study, we investigated the genetic evolution and characterized molecular markers of the recent H2N2 AIVs in LBMs in the Northeast USA. Phylogenetic analyses revealed that the LBM H2N2 lineage has evolved into three distinct subgroups (groups A.1, A.2, and A.3). The group A.1 viruses and some transient reassortants evolved through several independent reassortment events between the LBM H2N2 lineage and North American wild bird-origin AIVs. Separately, a group of phylogenetically distinct novel H2N2 viruses (group B) identified in LBMs completely originated from wild birds, independent from the previous LBM H2N2 lineage that has persisted since 2014. While no molecular evidence of mammalian adaptation was found, the novel H2N2 viruses in the LBM system underscore the importance of updated risk assessments for potential human transmission.
{"title":"Novel reassortant H2N2 low pathogenic avian influenza virus in live bird markets in the Northeastern United States, 2019-2023.","authors":"Sungsu Youk, Dong-Hun Lee, David E Swayne, Mary Lea Killian, Mia Kim Torchetti","doi":"10.1080/03079457.2024.2420712","DOIUrl":"10.1080/03079457.2024.2420712","url":null,"abstract":"<p><p>The H2N2 avian influenza viruses (AIV) have been reported in the Northeast United States of America (USA) live bird market (LBM) system since 2014. In this study, we investigated the genetic evolution and characterized molecular markers of the recent H2N2 AIVs in LBMs in the Northeast USA. Phylogenetic analyses revealed that the LBM H2N2 lineage has evolved into three distinct subgroups (groups A.1, A.2, and A.3). The group A.1 viruses and some transient reassortants evolved through several independent reassortment events between the LBM H2N2 lineage and North American wild bird-origin AIVs. Separately, a group of phylogenetically distinct novel H2N2 viruses (group B) identified in LBMs completely originated from wild birds, independent from the previous LBM H2N2 lineage that has persisted since 2014. While no molecular evidence of mammalian adaptation was found, the novel H2N2 viruses in the LBM system underscore the importance of updated risk assessments for potential human transmission.</p>","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"299-305"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-22DOI: 10.1080/03079457.2025.2503607
Sjaak de Wit, Damer P Blake
{"title":"Bart Rispens Research Award 2025 for the best paper published in <i>Avian Pathology</i> (volumes 52 and 53).","authors":"Sjaak de Wit, Damer P Blake","doi":"10.1080/03079457.2025.2503607","DOIUrl":"https://doi.org/10.1080/03079457.2025.2503607","url":null,"abstract":"","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"1"},"PeriodicalIF":2.5,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-12DOI: 10.1080/03079457.2025.2503607
Sjaak de Wit, Damer P Blake
{"title":"Bart Rispens Research Award 2025 for the best paper published in Avian Pathology (volumes 52 and 53).","authors":"Sjaak de Wit, Damer P Blake","doi":"10.1080/03079457.2025.2503607","DOIUrl":"https://doi.org/10.1080/03079457.2025.2503607","url":null,"abstract":"","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"1-2"},"PeriodicalIF":2.5,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The Duck Tembusu virus (DTMUV) was first reported in China in 2010 and has since caused substantial economic losses in the poultry breeding industry. In the autumn of 2022, an outbreak of an infectious disease resembling DTMUV was reported in Guangdong Province, China, which caused significantly high mortality in goose embryos, and decreased egg production. This study identified one strain of the new subgenotype 3 of DTMUV, designated as DTMUV GDZQ2022, responsible for these effects. Comprehensive genomic sequencing of this strain was conducted to analyse its genetic variations. Additionally, the isolated and purified virus was inoculated into goose embryos and goslings to assess its pathogenicity. The GDZQ2022 genome displayed over 88% nucleotide homology with other DTMUV strains from China and Southeast Asia. Phylogenetic analysis of the E gene classified GDZQ2022 within the subgenotype 3 of DTMUV. Pathogenicity experiments on goose embryos and goslings showed that the GDZQ2022 strain induced typical clinical signs of DTMUV, particularly severe neurological manifestations. Although GDZQ2022 exhibited high virulence in goose embryos, its virulence in goslings was minimal, resulting in a low mortality rate. Pathological examinations detected significant histological lesions in the brains, livers, and spleens of the infected goslings. In conclusion, this study presents the first evidence of a novel DTMUV strain proliferating among young geese in China, underscoring the genetic diversity of DTMUV and contributing to our understanding of the pathogenicity of the subgenotype 3 Tembusu virus in goose embryos and goslings.RESEARCH HIGHLIGHTSPathogenicity of subgenotype 3 duck Tembusu virus in goose embryos and goslings was shown for the first time.DTMUV GDZQ2022 strain is highly pathogenic in goose embryos.The virulence of the DTMUV GDZQ2022 strain in goslings is relatively mild.Infected goslings exhibit typical clinical manifestations, with a low mortality rate.
{"title":"Pathogenicity and transmissibility differences in goose-originated subgenotype 3 duck Tembusu virus in goose embryos and 3-day-old goslings.","authors":"Ziqiao Zhao, Junhong Ke, Mengfan Liu, Zuoxin Chen, Shuwen Li, Wuque Wei, Kun Mei, Shujian Huang","doi":"10.1080/03079457.2024.2373365","DOIUrl":"10.1080/03079457.2024.2373365","url":null,"abstract":"<p><p>The Duck Tembusu virus (DTMUV) was first reported in China in 2010 and has since caused substantial economic losses in the poultry breeding industry. In the autumn of 2022, an outbreak of an infectious disease resembling DTMUV was reported in Guangdong Province, China, which caused significantly high mortality in goose embryos, and decreased egg production. This study identified one strain of the new subgenotype 3 of DTMUV, designated as DTMUV GDZQ2022, responsible for these effects. Comprehensive genomic sequencing of this strain was conducted to analyse its genetic variations. Additionally, the isolated and purified virus was inoculated into goose embryos and goslings to assess its pathogenicity. The GDZQ2022 genome displayed over 88% nucleotide homology with other DTMUV strains from China and Southeast Asia. Phylogenetic analysis of the E gene classified GDZQ2022 within the subgenotype 3 of DTMUV. Pathogenicity experiments on goose embryos and goslings showed that the GDZQ2022 strain induced typical clinical signs of DTMUV, particularly severe neurological manifestations. Although GDZQ2022 exhibited high virulence in goose embryos, its virulence in goslings was minimal, resulting in a low mortality rate. Pathological examinations detected significant histological lesions in the brains, livers, and spleens of the infected goslings. In conclusion, this study presents the first evidence of a novel DTMUV strain proliferating among young geese in China, underscoring the genetic diversity of DTMUV and contributing to our understanding of the pathogenicity of the subgenotype 3 Tembusu virus in goose embryos and goslings.<b>RESEARCH HIGHLIGHTS</b>Pathogenicity of subgenotype 3 duck Tembusu virus in goose embryos and goslings was shown for the first time.DTMUV GDZQ2022 strain is highly pathogenic in goose embryos.The virulence of the DTMUV GDZQ2022 strain in goslings is relatively mild.Infected goslings exhibit typical clinical manifestations, with a low mortality rate.</p>","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"175-184"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142862573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}