Emerging Microbes & Infections最新文献_第7页

Paediatric varicella epidemiology in urban Beijing, China, 2014-2023. 2014-2023年北京城市儿童水痘流行病学

IF 8.4 2区医学

Emerging Microbes & Infections Pub Date : 2025-12-01 Epub Date: 2025-02-28 DOI: 10.1080/22221751.2025.2467773

Dan Yu, Wei Su, Miao Fan, Lu Lu, Xinyu Wang, Sheng Zhang, Qingjing Du, Lin Ma, Ying Liu, Kaihu Yao

引用次数: 0

SARS-CoV-2 enhances complement-mediated endothelial injury via the suppression of membrane complement regulatory proteins. SARS-CoV-2通过抑制膜补体调节蛋白增强补体介导的内皮损伤。

IF 8.4 2区医学

Emerging Microbes & Infections Pub Date : 2025-12-01 Epub Date: 2025-02-28 DOI: 10.1080/22221751.2025.2467781

Jian Wu, Sanpeng Xu, Zhiqing Li, Boyi Cong, Zongheng Yang, Zhichao Yang, Wanfeng Gao, Shuo Liu, Zhou Yu, Sheng Xu, Nan Li, Jin Hou, Guoping Wang, Xuetao Cao, Shuxun Liu

{"title":"SARS-CoV-2 enhances complement-mediated endothelial injury via the suppression of membrane complement regulatory proteins.","authors":"Jian Wu, Sanpeng Xu, Zhiqing Li, Boyi Cong, Zongheng Yang, Zhichao Yang, Wanfeng Gao, Shuo Liu, Zhou Yu, Sheng Xu, Nan Li, Jin Hou, Guoping Wang, Xuetao Cao, Shuxun Liu","doi":"10.1080/22221751.2025.2467781","DOIUrl":"10.1080/22221751.2025.2467781","url":null,"abstract":"Complement hyperactivation and thrombotic microangiopathy are closely associated with severe COVID-19. Endothelial dysfunction is a key mechanism underlying thrombotic microangiopathy. To address the relationship between endothelial injury, complement activation and thrombotic microangiopathy of severe COVID-19, we wonder whether, and if so, what and how SARS-CoV-2 factors make endothelial cells (ECs) sensitive to complement-mediated cytotoxicity. We revealed that multiple SARS-CoV-2 proteins enhanced complement-mediated cytotoxicity to ECs by inhibiting membrane complement regulatory proteins (CRPs) and enhancing the deposition of complement-recognizing component FCN1. By screening with CRISPR/Cas9-gRNA libraries, we identified that ADAMTS9, SYAP1, and HIGD1A as intrinsic regulators of CD59 on ECs, which were inhibited by the SARS-CoV-2 M, NSP16, and ORF9b proteins. IFN-γ, GM-CSF, and IFN-α upregulated CD55 and CD59, while IFN-γ antagonized the inhibition of CD59 by the three SARS-CoV-2 proteins. So, the deficiency of IFN-γ weakened the protection of ECs by CRPs against complement-mediated injury which may be enhanced during infection. Our findings illustrated the regulation of protection against complement-mediated attack on self-cells by SARS-CoV-2 infection and immune responses, providing insights into endothelial injury, thrombotic microangiopathy, and potential targets for treating severe COVID-19.","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2467781"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11873982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406514","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}

引用次数: 0

Dengue virus and lipid metabolism: unravelling the interplay for future therapeutic approaches. 登革病毒和脂质代谢：揭示未来治疗方法的相互作用。

IF 8.4 2区医学

Emerging Microbes & Infections Pub Date : 2025-12-01 Epub Date: 2025-04-09 DOI: 10.1080/22221751.2025.2477647

Ying Xie, Li Jiao, Qiangming Sun

引用次数: 0

Evaluation of global distribution, genetic evolution, and mammalian infectivity and pathogenicity of H13 and H16 avian influenza viruses. H13和H16禽流感病毒全球分布、遗传进化、哺乳动物传染性和致病性的评估。

IF 8.4 2区医学

Emerging Microbes & Infections Pub Date : 2025-12-01 Epub Date: 2025-03-28 DOI: 10.1080/22221751.2025.2482695

Xiang Li, Ao Li, Fengyi Qu, Yi Li, Fangyuan Chen, Xinru Lv, Qing An, Mengdan Fei, Hongyu Chen, Hongrui Liang, Xiaotian Zhang, Jinghao Li, Mingyuan Yu, Siyuan Qin, Linhong Xie, Shenglai Yin, Zheng Huang, Siyuan Yang, Heting Sun, Xiang Li, Hongliang Chai

{"title":"Evaluation of global distribution, genetic evolution, and mammalian infectivity and pathogenicity of H13 and H16 avian influenza viruses.","authors":"Xiang Li, Ao Li, Fengyi Qu, Yi Li, Fangyuan Chen, Xinru Lv, Qing An, Mengdan Fei, Hongyu Chen, Hongrui Liang, Xiaotian Zhang, Jinghao Li, Mingyuan Yu, Siyuan Qin, Linhong Xie, Shenglai Yin, Zheng Huang, Siyuan Yang, Heting Sun, Xiang Li, Hongliang Chai","doi":"10.1080/22221751.2025.2482695","DOIUrl":"10.1080/22221751.2025.2482695","url":null,"abstract":"H13 and H16 subtype avian influenza viruses (AIVs) typically infect Charadriiformes, are widely distributed throughout coastal regions worldwide, and pose a risk of spill-over to mammals. Systematic research on the epidemiology, transmission dynamics, and biological characteristics of these subtypes remains limited. To address this gap, we analyzed 20 years of wild bird influenza surveillance data from China integrated with global influenza database information to reconstruct the global spatiotemporal distribution, transmission dynamics and public health implications of H13 and H16. During influenza surveillance, 28 H13 and 19 H16 viruses were isolated. The phylogenetic trees for the H13 and H16 viruses revealed that both subtypes could be classified into three distinct groups. Viruses from H13 Group A, H13 Group C, and H16 Group C demonstrated frequent genetic exchanges and intercontinental transmission on a global scale. Mapping host migration revealed overlap between virus spread and host migration pathways. Our results suggest that host migration is a key driver of widespread distribution, cross-regional spread, and gene exchange for some H13 and H16 lineages. Virus isolates exhibit high genetic diversity with rich genotypic variation. Most isolates carry mammalian-adaptive mutations, such as the G228S mutation in the HA protein. H13 and H16 isolates of multiple genotypes infected mice without prior adaptation and exhibited varying tissue tropism. In summary, these findings indicate that host migration patterns are closely associated with the evolution of H13 and H16 AIVs. The potential risk of mammalian infection is highlighted, as viruses carrying mammalian-adaptive mutations may lead to new infection cases.","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2482695"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11956110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699929","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}

引用次数: 0

Origin of Neisseria meningitidis clonal complex 4821. 脑膜炎奈瑟菌克隆复合体4821的起源。

IF 8.4 2区医学

Emerging Microbes & Infections Pub Date : 2025-12-01 Epub Date: 2025-06-19 DOI: 10.1080/22221751.2025.2515461

Zhizhou Tan, Lin Xu, Jie Che, Juan Xu, Li Xu, Hairui Wang, Maojun Zhang, Biao Kan, Jianguo Xu, Zhujun Shao

{"title":"Origin of Neisseria meningitidis clonal complex 4821.","authors":"Zhizhou Tan, Lin Xu, Jie Che, Juan Xu, Li Xu, Hairui Wang, Maojun Zhang, Biao Kan, Jianguo Xu, Zhujun Shao","doi":"10.1080/22221751.2025.2515461","DOIUrl":"10.1080/22221751.2025.2515461","url":null,"abstract":"Neisseria meningitidis (N. meningitidis) is the causative agent of human invasive meningococcal disease (IMD). Clonal complex (CC) 4821 is a unique genetic cluster of N. meningitidis that emerged two decades ago in Anhui Province, China and became the predominant cluster. However, the evolutionary origin of CC4821 remains unclear. Herein, a distinct CC4821 clade was identified by a comprehensive cgMLST analysis of 26,801 N. meningitidis genomes. The CC4821 clade comprised 388 N. meningitidis isolates, with 364 assigned to CC4821, 1 assigned to CC8, and 23 unassigned (UA), as they could not be assigned to any defined CC. The phylogenetic analysis of the CC4821 clade revealed that six UA isolates, including the UA isolate NmR29026 collected in 1966 from Liaoning Province, China, occupied a basal position compared to all isolates within the CC4821 clade, indicating that CC4821 originated in the 1960s. Eight subclades (clades 1-8) were recognized within the CC4821 clade. Clades 1-4 have been present since the 1970s, while clades 5-8 emerged after the 2000s. Clade 5 represents a hyperinvasive lineage. N. meningitidis isolate HEB85-3, collected in 1985 in Hebei Province, China, exhibited the closest evolutionary relationship to clade 5, suggesting it is related to the origin of this hyperinvasive lineage. Our study reveals that CC4821 has emerged as the predominant cluster of N. meningitidis in China, representing the culmination of at least 60 years of continuous evolution in China, and is not solely attributable to the outbreak two decades ago.","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2515461"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12180329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144233539","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}

引用次数: 0

Mpox virus poxin-schlafen fusion protein suppresses innate antiviral response by sequestering STAT2. m痘病毒毒素-schlafen融合蛋白通过隔离STAT2抑制先天抗病毒反应。

IF 8.4 2区医学

Emerging Microbes & Infections Pub Date : 2025-12-01 Epub Date: 2025-03-18 DOI: 10.1080/22221751.2025.2477639

Pearl Chan, Zi-Wei Ye, Wenlong Zhao, Chon-Phin Ong, Xiao-Yu Sun, Pak-Hin Hinson Cheung, Dong-Yan Jin

{"title":"Mpox virus poxin-schlafen fusion protein suppresses innate antiviral response by sequestering STAT2.","authors":"Pearl Chan, Zi-Wei Ye, Wenlong Zhao, Chon-Phin Ong, Xiao-Yu Sun, Pak-Hin Hinson Cheung, Dong-Yan Jin","doi":"10.1080/22221751.2025.2477639","DOIUrl":"10.1080/22221751.2025.2477639","url":null,"abstract":"Mpox virus (MPXV) has to establish efficient interferon (IFN) antagonism for effective replication. MPXV-encoded IFN antagonists have not been fully elucidated. In this study, the IFN antagonism of poxin-schlafen (PoxS) fusion gene of MPXV was characterized. MPXV PoxS was capable of decreasing cGAS-produced 2'3'-cGAMP, like its ortholog poxin of vaccinia virus, which is the first known cytosolic nuclease that hydrolyses the 3'-5' bond of 2'3'-cyclic GMP-AMP (cGAMP). However, MPXV PoxS did not suppress cGAS-STING-mediated type I IFN production. Instead, MPXV PoxS antagonized basal and type I IFN-induced expression of IFN-stimulated genes such as OAS1, SAMD9, SAMD9L, ISG15, ISG56 and IFIT3. Consistently, MPXV PoxS inhibited both basal and type I IFN-stimulated activity of interferon-stimulated response elements, but did not affect activation of IFN-γ-activated sites. Mechanistically, MPXV PoxS interacted with STAT2 and sequestered it in the cytoplasm. Both the viral schlafen fusion and the active site of 2'3'-cGAMP nuclease were required for STAT2 sequestration and consequent suppression of IFN-stimulated gene expression. MPXV PoxS conferred resistance to the suppression of MPXV replication by type I IFN. Taken together, our findings suggested that MPXV PoxS counteracts host antiviral response by sequestering STAT2 to circumvent basal and type I IFN-induced expression of antiviral genes.","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2477639"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11921170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596608","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}

引用次数: 0

Unravelling distinct patterns of metagenomic surveillance and respiratory microbiota between two P1 genotypes of Mycoplasma pneumoniae. 揭示两种P1基因型肺炎支原体宏基因组监测和呼吸微生物群的不同模式。

IF 8.4 2区医学

Emerging Microbes & Infections Pub Date : 2025-12-01 Epub Date: 2025-01-13 DOI: 10.1080/22221751.2024.2449087

Hailong You, Bin Yang, Huifang Liu, Wencai Wu, Fei Yu, Nan Lin, WenJiao Yang, Bingxue Hu, Yong Liu, Hongyan Zou, Sijia Hao, Yunping Xiao, Teng Xu, Yanfang Jiang

{"title":"Unravelling distinct patterns of metagenomic surveillance and respiratory microbiota between two P1 genotypes of Mycoplasma pneumoniae.","authors":"Hailong You, Bin Yang, Huifang Liu, Wencai Wu, Fei Yu, Nan Lin, WenJiao Yang, Bingxue Hu, Yong Liu, Hongyan Zou, Sijia Hao, Yunping Xiao, Teng Xu, Yanfang Jiang","doi":"10.1080/22221751.2024.2449087","DOIUrl":"10.1080/22221751.2024.2449087","url":null,"abstract":"To unravel distinct patterns of metagenomic surveillance and respiratory microbiota between Mycoplasma pneumoniae (M. pneumoniae) P1-1 and P1-2 and to explore the impact of the COVID-19 pandemic on epidemiological features, we conducted a multicentre retrospective study which spanned 90,886 pneumonia patients, among which 3164 cases M. pneumoniae were identified. Our findings revealed a concurrent outbreak of M. pneumoniae, with the positivity rate rising sharply to 9.62% from July 2023, compared to the 0.16% to 4.06% positivity rate observed during the 2020-2022 COVID-19 pandemic. P1-1 had a higher odds ratio of co-detecting opportunistic pathogens. However, no significant differences were observed in the co-detection odds ratio between children and other age groups in P1-2. This study is the first to demonstrate differences in relative abundance, diversity of respiratory microbiota and co-detection rate of opportunistic pathogen between M. pneumoniae P1-1 and P1-2. Through bronchoalveolar lavage (BAL) metagenomic and host transcriptomic analyses, we identified variations in co-detection rates of M. pneumoniae P1-1 genotype with opportunistic pathogens like S. pneumoniae, alterations in respiratory microbiota composition, lung inflammation, and disruption of ciliary function. Consistent with the results of host transcriptome, we found that P1-1 infections were associated with significantly higher rates of requiring respiratory support and mechanical ventilation compared to P1-2 infections (Fisher's exact test, p-value = 0.035/0.004). Our study provides preliminary evidence of clinical severity between M. pneumoniae strains, underscoring the need for ongoing research and development of targeted therapeutic strategies.","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2449087"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930315","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}

引用次数: 0

Influenza A virus-induced interferon-alpha production by myeloid dendritic cells and macrophages requires productive infection. 甲型流感病毒诱导骨髓树突状细胞和巨噬细胞产生干扰素- α需要生产性感染。

IF 7.5 2区医学

Emerging Microbes & Infections Pub Date : 2025-12-01 Epub Date: 2025-09-16 DOI: 10.1080/22221751.2025.2556718

Marc A Niles, Stefanie Kronhart, Katharina E Decker, Patricia Gogesch, Bevan Sawatsky, Svenja Stock, Georg Kochs, Zoe Waibler, Martina Anzaghe

{"title":"Influenza A virus-induced interferon-alpha production by myeloid dendritic cells and macrophages requires productive infection.","authors":"Marc A Niles, Stefanie Kronhart, Katharina E Decker, Patricia Gogesch, Bevan Sawatsky, Svenja Stock, Georg Kochs, Zoe Waibler, Martina Anzaghe","doi":"10.1080/22221751.2025.2556718","DOIUrl":"10.1080/22221751.2025.2556718","url":null,"abstract":"Severe Influenza A virus (IAV) infections are accompanied by a cytokine storm with type I interferon (IFN) as the main driver. Besides epithelial cells, alveolar macrophages and infiltrating dendritic cells are target cells for IAV. IAV are classified into different strains, defined by their major surface glycoproteins haemagglutinin (HA) and neuraminidase (NA). So far, 19 HA subtypes and 11 NA subtypes are known. However, it is not well understood, why infection with certain IAV strains results in a cytokine storm with severe outcomes, while other IAV strains only cause mild infections. In order to address this question, we investigated six seasonal and five highly pathogenic avian IAV (HPAIV) strains using primary human ex vivo isolated plasmacytoid dendritic cells (pDC), as well as in vitro differentiated myeloid dendritic cells (mDC) and macrophages (type M1 and M2). Our data reveal that IFN-α production by mDC and macrophages but not by pDC is dependent on productive infection with the respective IAV strain. In contrast to IFN-α production in pDCs, IFN-α production by mDC as well as M1 and M2 macrophages is mainly induced by HPAIV strains, indicating that other immune cells apart from pDC might have an impact on induction of type I interferon as the main driver of the cytokine storm in the patients and the severity of the associated disease. Our findings may provide insights into the viral tropism and host response upon infection with different IAV strains and improve the understanding of the accompanied pathogenesis.","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2556718"},"PeriodicalIF":7.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12444950/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144947162","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}

引用次数: 0

Deletion of the African swine fever virus E120R gene completely attenuates its virulence by enhancing host innate immunity and impairing virus release. E120R基因缺失的非洲猪瘟病毒被完全减毒并在猪体内诱导部分保护性免疫。

IF 7.5 2区医学

Emerging Microbes & Infections Pub Date : 2025-12-01 Epub Date: 2025-09-20 DOI: 10.1080/22221751.2025.2555722

Boli Ma, Yiqian Jiang, Nan Li, Fengjie Wang, Qian Li, Huixian Yue, Yanyan Zhang, Rongliang Hu, Faming Miao

{"title":"Deletion of the African swine fever virus E120R gene completely attenuates its virulence by enhancing host innate immunity and impairing virus release.","authors":"Boli Ma, Yiqian Jiang, Nan Li, Fengjie Wang, Qian Li, Huixian Yue, Yanyan Zhang, Rongliang Hu, Faming Miao","doi":"10.1080/22221751.2025.2555722","DOIUrl":"10.1080/22221751.2025.2555722","url":null,"abstract":"African swine fever virus (ASFV) causes a lethal haemorrhagic disease in domestic pigs and poses a major threat to the global swine industry. Currently, no effective commercial vaccines or antiviral drugs are available for ASF control. In this study, we constructed a recombinant E120R gene-deleted virus, ASFV-ΔE120R, based on the highly virulent genotype II strain SY18, to investigate the role of the E120R gene. ASFV-ΔE120R exhibited impaired virion release and formed aberrant tubular structures, rendering viral particles more susceptible to neutralization by convalescent pig sera. ASFV-ΔE120R induced higher levels of transcription of Cytokines, chemokines, and interferon-regulated genes in porcine alveolar macrophages compared with ASFV-WT. In vivo safety evaluation demonstrated that piglets immunized with 5 × 10⁶ TCID₅₀ of ASFV-ΔE120R exhibited no clinical signs or viral nucleic acid in tissues at necropsy on days 4, 7, 10, and 14 post-immunization. Two immunizations at the same dose, 21 days apart, also induced no clinical signs or viral shedding during a 28-day observation. Immunogenicity analysis showed that ASFV-ΔE120R elicited p54-specific antibodies and IFN-γ-secreting PBMC responses. Upon challenge with parental ASFV SY18, two of five pigs (40%) survived, showing elevated antibody levels, IFN-γ-secreting PBMCs, and increased CD8+ IFN-γ+ T cells. Moreover, Cytokines and interferon-stimulated genes were significantly upregulated in survivors. In summary, ASFV-ΔE120R is fully attenuated, safe, and induces both humoral and cellular immune responses, highlighting pE120R as a rational target for ASF vaccine development.","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2555722"},"PeriodicalIF":7.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12451965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144947167","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}

引用次数: 0

Reassortment of newly emergent clade 2.3.4.4b A(H5N1) highly pathogenic avian influenza A viruses in Bangladesh. 孟加拉国新出现的 2.3.4.4b 支系 A(H5N1)高致病性甲型禽流感病毒的重新组合。

IF 8.4 2区医学

Emerging Microbes & Infections Pub Date : 2025-12-01 Epub Date: 2024-12-09 DOI: 10.1080/22221751.2024.2432351

Subrata Barman, Jasmine C M Turner, M Kamrul Hasan, Sharmin Akhtar, Trushar Jeevan, John Franks, David Walker, Nabanita Mukherjee, Patrick Seiler, Lisa Kercher, Pamela McKenzie, Robert G Webster, Mohammed M Feeroz, Richard J Webby

{"title":"Reassortment of newly emergent clade 2.3.4.4b A(H5N1) highly pathogenic avian influenza A viruses in Bangladesh.","authors":"Subrata Barman, Jasmine C M Turner, M Kamrul Hasan, Sharmin Akhtar, Trushar Jeevan, John Franks, David Walker, Nabanita Mukherjee, Patrick Seiler, Lisa Kercher, Pamela McKenzie, Robert G Webster, Mohammed M Feeroz, Richard J Webby","doi":"10.1080/22221751.2024.2432351","DOIUrl":"10.1080/22221751.2024.2432351","url":null,"abstract":"ABSTRACTAvian influenza active surveillance was conducted in Bangladesh from January 2022 to November 2023 in live-poultry markets (LPMs) and Tanguar Haor wetlands. The predominant viruses circulating in LPMs were low pathogenic avian influenza (LPAI) A(H9N2) and clade 2.3.2.1a highly pathogenic avian influenza (HPAI) A(H5N1) viruses. Non-H9N2 LPAIs were found at Tanguar Haor and at a lower prevalence in LPMs. Starting from June 2023, we detected novel genotypes of clade 2.3.4.4b A(H5N1) viruses from ducks in LPMs. The HA, NA, and M genes of these viruses are related to those of 2020 European clade 2.3.4.4b H5N1 viruses such as A/Eurasian Wigeon/Netherlands/1/2020 (Netherlands/1). However, analyses of the other five gene segments' sequences identified three distinct genotypes (BD-G2, BD-G3, and BD-G4). BD-G2 viruses were closely related to the clade 2.3.4.4b H5N1 viruses that have been detected in Japan and nearby regions since November 2022. BD-G3 viruses were reassortants, with gene segments from other Eurasian LPAI viruses. BD-G4 viruses were similar to BD-G2 viruses, but their NS gene was accrued from contemporary Bangladeshi clade 2.3.2.1a A(H5N1) viruses. The ability of any of the clade 2.3.4.4b viruses to displace the long-entrenched 2.3.2.1a A(H5N1) viruses in Bangladesh is unknown.","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2432351"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11632930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709666","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}

引用次数: 0