Emerging Microbes & Infections最新文献

{"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":"<p><p>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.</p>","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}

{"title":"Eukaryotic RNA binding protein hnRNPH1 suppresses influenza A virus replication through interaction with virus NS1 protein.","authors":"Jinyu Wang, Yang Zhang, Lishan Sun, Zihan Wang, Cui Hao, Wei Wang","doi":"10.1080/22221751.2025.2477645","DOIUrl":"10.1080/22221751.2025.2477645","url":null,"abstract":"<p><p>The NS1 protein of influenza A virus (IAV) is a multi-functional protein which can antagonize host immune system and facilitate viral replication by interacting with host factors. However, the novel partners in host cells interacting with NS1 need to be fully elucidated. In the current study, we identified hnRNPH1 as a novel binding partner of NS1 to regulate IAV replication. Notably, overexpression of hnRNPH1 decreased IAV multiplication, while knockdown of hnRNPH1 enhanced IAV replication. hnRNPH1 can interact with NS1 to change the intracellular localization and splicing function of NS1, and impact IAV replication through interacting with p53 to regulate cell apoptosis. In addition, the RBD domain of NS1 and the RRM and NLS regions of hnRNPH1 may be the major sites for their interaction. In summary, our studies identified hnRNPH1 as a novel NS1-binding protein and elucidated its regulatory roles in IAV replication, which will provide new insights into the roles of NS1 binding proteins, and give a reference for anti-IAV therapy based on NS1-host interaction.</p>","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2477645"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572381","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}

{"title":"Influenza H5Nx viruses are susceptible to MEK1/2 inhibition by zapnometinib.","authors":"André Schreiber, Nicole Oberberg, Benjamin Ambrosy, Franziska Rodner, Sriram Kumar, Duygu Merve Caliskan, Linda Brunotte, Martin Beer, Stephan Ludwig","doi":"10.1080/22221751.2025.2471022","DOIUrl":"10.1080/22221751.2025.2471022","url":null,"abstract":"<p><p>Highly pathogenic avian influenza A viruses (HPAIV) pose a significant threat to both animal and human health. These viruses have the potential to cause severe respiratory and systemic infections in birds and several mammalian species. The recent global outbreak of the H5N1 clade 2.3.4.4b spread in wild and domestic birds is now considered to be a panzoonosis. Spillover events in dairy cattle farms in the U.S. have highlighted the urgent need for effective antiviral therapies, especially in view of human infections. This study investigates the selective MEK1/2 inhibitor zapnometinib (ZMN) as a potential antiviral agent against HPAIVs. Our <i>in vitro</i> experiments demonstrate that ZMN significantly impairs viral replication across multiple HPAIV strains, including H5N1 clade 2.3.4.4b in cell lines and primary bronchial epithelial cells. The mechanism of action is based on the nuclear retention of newly produced viral ribonucleoprotein complexes (vRNP), when the MEK/ERK/RSK1 kinase cascade is inhibited. We furthermore could show, that ZMN not only acts antiviral in a standalone treatment but has synergistic potential when used in combination with direct-acting antivirals like oseltamivir or baloxavir. Therefore, ZMN treatment offers a promising strategy for future antiviral development.</p>","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2471022"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143457275","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}

{"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":"<p><p>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.</p>","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}

{"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":"<p><p><b>ABSTRACT</b>Avian 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.</p>","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}

{"title":"The haemagglutinin gene of bovine-origin H5N1 influenza viruses currently retains receptor-binding and pH-fusion characteristics of avian host phenotype.","authors":"Jiayun Yang, Mehnaz Qureshi, Reddy Kolli, Thomas P Peacock, Jean-Remy Sadeyen, Toby Carter, Samuel Richardson, Rebecca Daines, Wendy S Barclay, Ian H Brown, Munir Iqbal","doi":"10.1080/22221751.2025.2451052","DOIUrl":"10.1080/22221751.2025.2451052","url":null,"abstract":"<p><p>Clade 2.3.4.4b H5N1 high pathogenicity avian influenza virus (HPAIV) has caused a panzootic affecting all continents except Australia, expanding its host range to several mammalian species. In March 2024, H5N1 HPAIV was first detected in dairy cattle and goats in the United States. Over 891 dairy farms across 16 states have tested positive until 25 December 2024, with zoonotic infections reported among dairy workers. This raises concerns about the virus undergoing evolutionary changes in cattle that could enhance its zoonotic potential. The Influenza glycoprotein haemagglutinin (HA) facilitates entry into host cells through receptor binding and pH-induced fusion with cellular membranes. Adaptive changes in HA modulate virus-host cell interactions. This study compared the HA genes of cattle and goat H5N1 viruses with the dominant avian-origin clade 2.3.4.4b H5N1 in the United Kingdom, focusing on receptor binding, pH fusion, and thermostability. All the tested H5N1 viruses showed binding exclusively to avian-like receptors, with a pH fusion of 5.9, outside the pH range associated with efficient human airborne transmissibility (pH 5.0-5.5). We further investigated the impact of emerging HA substitutions seen in the ongoing cattle outbreaks, but saw little phenotypic difference, with continued exclusive binding to avian-like receptor analogues and pHs of fusion above 5.8. This suggests that the HA genes from the cattle and goat outbreaks do not pose an enhanced threat compared to circulating avian viruses. However, given the rapid evolution of H5 viruses, continuous monitoring and updated risk assessments remain essential to understanding virus zoonotic and pandemic risks.</p>","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2451052"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970155","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}

{"title":"The epidemiology and gene mutation characteristics of pyrazinamide-resistant <i>Mycobacterium tuberculosis</i> clinical isolates in Southern China.","authors":"Nan Wang, Fanrong Meng, Li Deng, Ling Wu, Yu Yang, Hua Li, Yuanjin Chen, Zeyou Wei, Bei Xie, Lan Gong, Qun Niu, Jie Lei, Junwen Gao, Bo Huang, Qi Wang, Xiaomin Lai, Zhihui Liu, Jinxing Hu","doi":"10.1080/22221751.2024.2447607","DOIUrl":"10.1080/22221751.2024.2447607","url":null,"abstract":"<p><p>This study investigates the epidemic trend of pyrazinamide (PZA)-resistant tuberculosis in Southern China over 11 years (2012-2022) and evaluates the mutation characteristics of PZA resistance-related genes (<i>pncA, rpsA,</i> and <i>panD</i>) in clinical <i>Mycobacterium tuberculosis</i> (<i>M. tuberculosis</i>) isolates. To fulfil these goals, we analyzed the phenotypic PZA resistance characteristics of 14,927 clinical isolates for which Bactec MGIT 960 PZA drug susceptibility testing (DST) results were available, revealing that 2,054 (13.76%) isolates were resistant to PZA. After evaluating the annual variation in the PZA resistance rate among tuberculosis cases in this region, it was observed that it decreased from 37.21% to 6.45% throughout the initial 7 years (2012-2018) and then increased from 8.01% to 12.12% over the subsequent 4 years (2019-2022). Sequences of <i>pncA</i> were obtained from 402 clinical <i>M. tuberculosis</i> complex isolates. For <i>rpsA</i> and <i>panD,</i> sequences were obtained from 360 clinical <i>M. tuberculosis</i> complex isolates. Mutations in <i>pncA</i> were found in 8 out of 223 PZA-sensitive isolates (3.59%) and 105 of 179 (58.66%) PZA-resistant isolates. Conversely, non-synonymous mutations in <i>rpsA</i> were identified in 5 of 137 (3.65%) PZA-resistant isolates, whereas the mutation ratio of <i>rpsA</i> among PZA-sensitive isolates was high at 14.03% (31/221). This difference in the <i>rpsA</i> mutation rate was statistically significant (<i>P = 0.001</i>, chi-square test). No <i>panD</i> mutations were observed in the 137 PZA-resistant isolates, whereas two PZA-sensitive isolates harboured point mutations in <i>panD</i>, including one nonsense mutation (C433 T) and another C-69 T mutation. These findings indicate that <i>rpsA</i> and <i>panD</i> may not significantly contribute to the development of PZA resistance in clinical <i>M. tuberculosis</i> isolates.</p>","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2447607"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11721771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142913559","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}

{"title":"Emerging antifungal resistance in <i>Trichophyton mentagrophytes</i>: insights from susceptibility profiling and genetic mutation analysis.","authors":"Yakun Shao, Jin Shao, Sybren de Hoog, Paul Verweij, Lin Bai, Riina Richardson, Malcolm Richardson, Zhe Wan, Ruoyu Li, Jin Yu, Yinggai Song","doi":"10.1080/22221751.2025.2450026","DOIUrl":"10.1080/22221751.2025.2450026","url":null,"abstract":"<p><p><b>ABSTRACT</b><i>Trichophyton</i> species, the leading cause of dermatophytosis globally, are increasingly resistant to antifungal treatments, concerns about effective management strategies. In light of the absence of established resistance criteria for terbinafine and azoles, coupled with a dearth of research on resistance mechanisms in <i>Trichophyton</i>, antifungal susceptibility and drug resistance gene diversity were analyzed across 64 <i>T. mentagrophytes</i>, 65 <i>T. interdigitale</i>, and 2 <i>T. indotineae</i> isolates collected in China between 1999 and 2024 and 101 published <i>T. indotineae</i> strains. Analyses of the minimum inhibitory concentrations (MICs) of terbinafine, itraconazole, voriconazole, posaconazole, and isavuconazole revealed a concerning increase in <i>T. indotineae</i> with terbinafine resistance, including two novel isolates from China. Compared with <i>T. interdigitale, T. mentagrophytes</i> presented higher terbinafine MICs but similar azole susceptibility. Notably, 27 <i>T. interdigitale</i> isolates were classified as non-wild-type for terbinafine. Genetic diversity was analyzed for the <i>SQLE</i>, <i>CYP51A</i> and <i>CYP51B</i> gene. Specifically, <i>T. indotineae</i> isolates presented SQLE protein changes linked to terbinafine resistance. SQLE diversity was linked to terbinafine sensitivity, whereas alterations in CYP51A were associated with itraconazole sensitivity, with notable statistical significance evident across various protein isoforms. The relationship between protein diversity and drug sensitivity is presented in detail. Together, these findings highlight a growing prevalence of antibiotic resistance among <i>Trichophyton</i> and identify potential target genes for new therapies, underscoring the need for ongoing monitoring and offering directions for novel therapeutics.</p>","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2450026"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11740296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920841","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}

{"title":"Replication kinetics, pathogenicity and virus-induced cellular responses of cattle-origin influenza A(H5N1) isolates from Texas, United States.","authors":"Ahmed Mostafa, Ramya S Barre, Anna Allué-Guardia, Ruby A Escobedo, Vinay Shivanna, Hussin Rothan, Esteban M Castro, Yao Ma, Anastasija Cupic, Nathaniel Jackson, Mahmoud Bayoumi, Jordi B Torrelles, Chengjin Ye, Adolfo García-Sastre, Luis Martinez-Sobrido","doi":"10.1080/22221751.2024.2447614","DOIUrl":"10.1080/22221751.2024.2447614","url":null,"abstract":"<p><p>The host range of HPAIV H5N1 was recently expanded to include ruminants, particularly dairy cattle in the United States (US). Shortly after, human H5N1 infection was reported in a dairy worker in Texas following exposure to infected cattle. Herein, we rescued the cattle-origin influenza A/bovine/Texas/24-029328-02/2024(H5N1, rHPbTX) and A/Texas/37/2024(H5N1, rHPhTX) viruses, identified in dairy cattle and human, respectively, and their low pathogenic forms, rLPbTX and rLPhTX, with monobasic HA cleavage sites. Intriguingly, rHPhTX replicated more efficiently than rHPbTX in mammalian and avian cells. Still, variations in the PA and NA proteins didn't affect their antiviral susceptibility to PA and NA inhibitors. Unlike rHPbTX and rLPbTX, both rHPhTX and rLPhTX exhibited higher pathogenicity and efficient replication in infected C57BL/6J mice. The lungs of rHPhTX-infected mice produced higher inflammatory cytokines/chemokines than rHPbTX-infected mice. Our results highlight the potential risk of HPAIV H5N1 virus adaptation in human and/or dairy cattle during the current multistate/multispecies outbreak in the US.</p>","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":" ","pages":"2447614"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11721806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893000","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}

{"title":"Correction.","authors":"","doi":"10.1080/22221751.2025.2467547","DOIUrl":"10.1080/22221751.2025.2467547","url":null,"abstract":"","PeriodicalId":11602,"journal":{"name":"Emerging Microbes & Infections","volume":"14 1","pages":"2467547"},"PeriodicalIF":8.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143472395","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}