Pub Date : 2025-01-02DOI: 10.1038/s41564-024-01879-4
Jérémy Dufloo, Iván Andreu-Moreno, Jorge Moreno-García, Ana Valero-Rello, Rafael Sanjuán
Cross-species transmission of animal viruses poses a threat to human health. However, systematic experimental assessments of these risks remain scarce. A critical step in viral infection is cellular internalization mediated by viral receptor-binding proteins (RBPs). Here we constructed viral pseudotypes bearing the RBPs of 102 enveloped RNA viruses and assayed their infectivity across 5,202 RBP–cell combinations. This showed that most of the tested viruses have the potential to enter human cells. Pseudotype infectivity varied widely among the 14 viral families examined and was influenced by RBP characteristics, host of origin and target cell type. Cellular gene expression data revealed that the availability of specific cell-surface receptors is not necessarily the main factor limiting viral entry and that additional host factors must be considered. Altogether, these results suggest weak interspecies barriers in the early stages of infection and advance our understanding of the molecular interactions driving viral zoonosis. Functional systematic pseudotype virus-based analysis of the ability of diverse animal viruses to enter into a panel of well-characterized human cell lines shows a broad compatibility between animal virus receptor-binding proteins and human cell entry factors.
{"title":"Receptor-binding proteins from animal viruses are broadly compatible with human cell entry factors","authors":"Jérémy Dufloo, Iván Andreu-Moreno, Jorge Moreno-García, Ana Valero-Rello, Rafael Sanjuán","doi":"10.1038/s41564-024-01879-4","DOIUrl":"10.1038/s41564-024-01879-4","url":null,"abstract":"Cross-species transmission of animal viruses poses a threat to human health. However, systematic experimental assessments of these risks remain scarce. A critical step in viral infection is cellular internalization mediated by viral receptor-binding proteins (RBPs). Here we constructed viral pseudotypes bearing the RBPs of 102 enveloped RNA viruses and assayed their infectivity across 5,202 RBP–cell combinations. This showed that most of the tested viruses have the potential to enter human cells. Pseudotype infectivity varied widely among the 14 viral families examined and was influenced by RBP characteristics, host of origin and target cell type. Cellular gene expression data revealed that the availability of specific cell-surface receptors is not necessarily the main factor limiting viral entry and that additional host factors must be considered. Altogether, these results suggest weak interspecies barriers in the early stages of infection and advance our understanding of the molecular interactions driving viral zoonosis. Functional systematic pseudotype virus-based analysis of the ability of diverse animal viruses to enter into a panel of well-characterized human cell lines shows a broad compatibility between animal virus receptor-binding proteins and human cell entry factors.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"10 2","pages":"405-419"},"PeriodicalIF":20.5,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41564-024-01879-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-30DOI: 10.1038/s41564-024-01893-6
A predictive model developed using machine learning, high-throughput sequencing of the microbiomes associated with seed tubers and drone imaging of the crops growing from the tubers can forecast the performance of potato plants based on the microbiome composition of their seed tubers. In addition, this model can identify the best microbial predictors of potato plant growth.
{"title":"Potato crop performance is predicted by tuber microbiome","authors":"","doi":"10.1038/s41564-024-01893-6","DOIUrl":"10.1038/s41564-024-01893-6","url":null,"abstract":"A predictive model developed using machine learning, high-throughput sequencing of the microbiomes associated with seed tubers and drone imaging of the crops growing from the tubers can forecast the performance of potato plants based on the microbiome composition of their seed tubers. In addition, this model can identify the best microbial predictors of potato plant growth.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"10 1","pages":"8-9"},"PeriodicalIF":20.5,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-27DOI: 10.1038/s41564-024-01872-x
Yang Song, Elisa Atza, Juan J. Sánchez-Gil, Doretta Akkermans, Ronnie de Jonge, Peter G. H. de Rooij, David Kakembo, Peter A. H. M. Bakker, Corné M. J. Pieterse, Neil V. Budko, Roeland L. Berendsen
Potato vigour, the growth potential of seed potatoes, is a key agronomic trait that varies significantly across production fields due to factors such as genetic background and environmental conditions. Seed tuber microbiomes are thought to influence plant health and crop performance, yet the precise relationships between microbiome composition and potato vigour remain unclear. Here we conducted microbiome sequencing on seed tuber eyes and heel ends from 6 potato varieties grown in 240 fields. By using time-resolved drone imaging of three trial fields in the next season to track crop development, we were able to link microbiome composition with potato vigour. We used microbiome data at varying taxonomic resolutions to build random forest predictive models and found that amplicon sequence variants provided the highest predictive accuracy for potato vigour. The model revealed variety-specific relationships between the seed tuber microbiome and next season’s crop vigour in independent trial fields. With a coefficient of determination value of 0.69 for the best-performing variety, the model accurately predicted vigour in seed tubers from fields not previously included in the analysis. Moreover, the model identified key microbial indicators of vigour from which a Streptomyces, an Acinetobacter and a Cellvibrio amplicon sequence variant stood out as the most important contributors to the model’s accuracy. This study shows that seed potato vigour can be reliably predicted based on the microbiota associated with seed tuber eyes, potentially guiding future microbiome-informed breeding strategies. Time-resolved drone imaging of potato crop development and seed tuber microbiome data can be used to predict potato vigour, or growth potential, in next-season crops in trial fields.
{"title":"Seed tuber microbiome can predict growth potential of potato varieties","authors":"Yang Song, Elisa Atza, Juan J. Sánchez-Gil, Doretta Akkermans, Ronnie de Jonge, Peter G. H. de Rooij, David Kakembo, Peter A. H. M. Bakker, Corné M. J. Pieterse, Neil V. Budko, Roeland L. Berendsen","doi":"10.1038/s41564-024-01872-x","DOIUrl":"10.1038/s41564-024-01872-x","url":null,"abstract":"Potato vigour, the growth potential of seed potatoes, is a key agronomic trait that varies significantly across production fields due to factors such as genetic background and environmental conditions. Seed tuber microbiomes are thought to influence plant health and crop performance, yet the precise relationships between microbiome composition and potato vigour remain unclear. Here we conducted microbiome sequencing on seed tuber eyes and heel ends from 6 potato varieties grown in 240 fields. By using time-resolved drone imaging of three trial fields in the next season to track crop development, we were able to link microbiome composition with potato vigour. We used microbiome data at varying taxonomic resolutions to build random forest predictive models and found that amplicon sequence variants provided the highest predictive accuracy for potato vigour. The model revealed variety-specific relationships between the seed tuber microbiome and next season’s crop vigour in independent trial fields. With a coefficient of determination value of 0.69 for the best-performing variety, the model accurately predicted vigour in seed tubers from fields not previously included in the analysis. Moreover, the model identified key microbial indicators of vigour from which a Streptomyces, an Acinetobacter and a Cellvibrio amplicon sequence variant stood out as the most important contributors to the model’s accuracy. This study shows that seed potato vigour can be reliably predicted based on the microbiota associated with seed tuber eyes, potentially guiding future microbiome-informed breeding strategies. Time-resolved drone imaging of potato crop development and seed tuber microbiome data can be used to predict potato vigour, or growth potential, in next-season crops in trial fields.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"10 1","pages":"28-40"},"PeriodicalIF":20.5,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-23DOI: 10.1038/s41564-024-01847-y
Researchers show that the dynamics of metabolomic rearrangement dictate the growth response of bacteria and fungi to rapid changes in temperature. Single-cell microscopy revealed a mechanism for transient memory of previous temperatures and indicated that these responses are generally conserved, advancing our understanding of microbial behaviour in fluctuating environments.
{"title":"How microbial growth adapts to temperature shifts","authors":"","doi":"10.1038/s41564-024-01847-y","DOIUrl":"10.1038/s41564-024-01847-y","url":null,"abstract":"Researchers show that the dynamics of metabolomic rearrangement dictate the growth response of bacteria and fungi to rapid changes in temperature. Single-cell microscopy revealed a mechanism for transient memory of previous temperatures and indicated that these responses are generally conserved, advancing our understanding of microbial behaviour in fluctuating environments.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"10 1","pages":"12-13"},"PeriodicalIF":20.5,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142874048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-17DOI: 10.1038/s41564-024-01873-w
Chao Lei, Chao Luo, Zhishan Xu, Shu Ding, Mukesh K. Sriwastva, Gerald Dryden, Ting Wang, Manman Xu, Yi Tan, Qilong Wang, Xiaozhong Yang, Craig J. McClain, Zhongbin Deng
Inflammatory bowel disease is associated with several genetic risk loci. Loss-of-function mutation in the α1,2-fucosyltransferase (fut2) gene, which alters fucosylation on the surface of intestinal epithelial cells, is one example. However, whether bacterial fucosylation can contribute to gut inflammation is unclear. Here we show that host fucosylation status influences fucosylation biosynthesis by gut commensal bacteria. Mice colonized with faecal microbiota of Fut2 knockout mice or Bacteroides fragilis with lower surface fucosylation are predisposed to colitis. This was supported by human cohort data showing that bacterial fucosylation levels decrease in patients with inflammatory bowel disease and correlate with intestinal inflammation. Using a mouse model for Bacteroides fragilis to explore the role of fucosylation in gut immunity, we show that the fucosylation status of epithelial cells and bacteria is critical for maintaining B cell responses in the gut. Host-derived and dietary fucose mediate immunoglobulin A (IgA) recognition of gut microbiota, and this interaction facilitates the translocation of commensals to Peyer’s patches and alters the immune landscape of Peyer’s patches with increased germinal centre B cells and IgA-secreting antigen-specific B cells. Finally, dietary fucose enhances the IgA response against Salmonella and protects against systemic bacterial dissemination. This highlights the role of host and bacterial fucosylation in maintaining IgA homeostasis and immune escape mechanisms. Bacterial and host fucosylation protect against colitis by maintaining the IgA B cell response in the mouse gut.
炎症性肠病与几个遗传风险基因位点有关。例如，α1,2-岩藻糖基转移酶（fut2）基因的功能缺失突变会改变肠上皮细胞表面的岩藻糖基化。然而，细菌的岩藻糖基化是否会导致肠道炎症还不清楚。在这里，我们发现宿主的岩藻糖基化状态会影响肠道共生细菌的岩藻糖基化生物合成。小鼠定植于表面岩藻糖基化较低的 Fut2 基因敲除小鼠或脆弱拟杆菌的粪便微生物群后，易患结肠炎。人类队列数据也证明了这一点，这些数据显示，炎症性肠病患者体内的细菌岩藻糖基化水平降低，并与肠道炎症相关。我们利用脆弱拟杆菌小鼠模型来探索岩藻糖基化在肠道免疫中的作用，结果表明上皮细胞和细菌的岩藻糖基化状态对于维持肠道中的 B 细胞反应至关重要。宿主来源的岩藻糖和膳食岩藻糖介导了肠道微生物群的免疫球蛋白 A（IgA）识别，这种相互作用促进了共生菌向佩耶氏斑块的转移，并改变了佩耶氏斑块的免疫格局，增加了生殖中心 B 细胞和分泌 IgA 的抗原特异性 B 细胞。最后，膳食岩藻糖可增强针对沙门氏菌的 IgA 反应，并防止细菌全身扩散。这凸显了宿主和细菌岩藻糖基化在维持 IgA 平衡和免疫逃逸机制中的作用。
{"title":"Bacterial and host fucosylation maintain IgA homeostasis to limit intestinal inflammation in mice","authors":"Chao Lei, Chao Luo, Zhishan Xu, Shu Ding, Mukesh K. Sriwastva, Gerald Dryden, Ting Wang, Manman Xu, Yi Tan, Qilong Wang, Xiaozhong Yang, Craig J. McClain, Zhongbin Deng","doi":"10.1038/s41564-024-01873-w","DOIUrl":"10.1038/s41564-024-01873-w","url":null,"abstract":"Inflammatory bowel disease is associated with several genetic risk loci. Loss-of-function mutation in the α1,2-fucosyltransferase (fut2) gene, which alters fucosylation on the surface of intestinal epithelial cells, is one example. However, whether bacterial fucosylation can contribute to gut inflammation is unclear. Here we show that host fucosylation status influences fucosylation biosynthesis by gut commensal bacteria. Mice colonized with faecal microbiota of Fut2 knockout mice or Bacteroides fragilis with lower surface fucosylation are predisposed to colitis. This was supported by human cohort data showing that bacterial fucosylation levels decrease in patients with inflammatory bowel disease and correlate with intestinal inflammation. Using a mouse model for Bacteroides fragilis to explore the role of fucosylation in gut immunity, we show that the fucosylation status of epithelial cells and bacteria is critical for maintaining B cell responses in the gut. Host-derived and dietary fucose mediate immunoglobulin A (IgA) recognition of gut microbiota, and this interaction facilitates the translocation of commensals to Peyer’s patches and alters the immune landscape of Peyer’s patches with increased germinal centre B cells and IgA-secreting antigen-specific B cells. Finally, dietary fucose enhances the IgA response against Salmonella and protects against systemic bacterial dissemination. This highlights the role of host and bacterial fucosylation in maintaining IgA homeostasis and immune escape mechanisms. Bacterial and host fucosylation protect against colitis by maintaining the IgA B cell response in the mouse gut.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"10 1","pages":"126-143"},"PeriodicalIF":20.5,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142832156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-13DOI: 10.1038/s41564-024-01841-4
Benjamin D. Knapp, Lisa Willis, Carlos Gonzalez, Harsh Vashistha, Joanna Jammal-Touma, Mikhail Tikhonov, Jeffrey Ram, Hanna Salman, Josh E. Elias, Kerwyn Casey Huang
Temperature is a key determinant of microbial behaviour and survival in the environment and within hosts. At intermediate temperatures, growth rate varies according to the Arrhenius law of thermodynamics, which describes the effect of temperature on the rate of a chemical reaction. However, the mechanistic basis for this behaviour remains unclear. Here we use single-cell microscopy to show that Escherichia coli exhibits a gradual response to temperature upshifts with a timescale of ~1.5 doublings at the higher temperature. The response was largely independent of initial or final temperature and nutrient source. Proteomic and genomic approaches demonstrated that adaptation to temperature is independent of transcriptional, translational or membrane fluidity changes. Instead, an autocatalytic enzyme network model incorporating temperature-sensitive Michaelis–Menten kinetics recapitulates all temperature-shift dynamics through metabolome rearrangement, resulting in a transient temperature memory. The model successfully predicts alterations in the temperature response across nutrient conditions, diverse E. coli strains from hosts with different body temperatures, soil-dwelling Bacillus subtilis and fission yeast. In sum, our model provides a mechanistic framework for Arrhenius-dependent growth. Growth rate dynamics after temperature shifts can be explained by metabolic rearrangement due to temperature-sensitive enzyme activities in bacteria and yeast.
{"title":"Metabolic rearrangement enables adaptation of microbial growth rate to temperature shifts","authors":"Benjamin D. Knapp, Lisa Willis, Carlos Gonzalez, Harsh Vashistha, Joanna Jammal-Touma, Mikhail Tikhonov, Jeffrey Ram, Hanna Salman, Josh E. Elias, Kerwyn Casey Huang","doi":"10.1038/s41564-024-01841-4","DOIUrl":"10.1038/s41564-024-01841-4","url":null,"abstract":"Temperature is a key determinant of microbial behaviour and survival in the environment and within hosts. At intermediate temperatures, growth rate varies according to the Arrhenius law of thermodynamics, which describes the effect of temperature on the rate of a chemical reaction. However, the mechanistic basis for this behaviour remains unclear. Here we use single-cell microscopy to show that Escherichia coli exhibits a gradual response to temperature upshifts with a timescale of ~1.5 doublings at the higher temperature. The response was largely independent of initial or final temperature and nutrient source. Proteomic and genomic approaches demonstrated that adaptation to temperature is independent of transcriptional, translational or membrane fluidity changes. Instead, an autocatalytic enzyme network model incorporating temperature-sensitive Michaelis–Menten kinetics recapitulates all temperature-shift dynamics through metabolome rearrangement, resulting in a transient temperature memory. The model successfully predicts alterations in the temperature response across nutrient conditions, diverse E. coli strains from hosts with different body temperatures, soil-dwelling Bacillus subtilis and fission yeast. In sum, our model provides a mechanistic framework for Arrhenius-dependent growth. Growth rate dynamics after temperature shifts can be explained by metabolic rearrangement due to temperature-sensitive enzyme activities in bacteria and yeast.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"10 1","pages":"185-201"},"PeriodicalIF":20.5,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142815713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-04DOI: 10.1038/s41564-024-01900-w
Qi Su, Oscar W. H. Wong, Wenqi Lu, Yating Wan, Lin Zhang, Wenye Xu, Moses K. T. Li, Chengyu Liu, Chun Pan Cheung, Jessica Y. L. Ching, Pui Kuan Cheong, Ting Fan Leung, Sandra Chan, Patrick Leung, Francis K. L. Chan, Siew C. Ng
{"title":"Author Correction: Multikingdom and functional gut microbiota markers for autism spectrum disorder","authors":"Qi Su, Oscar W. H. Wong, Wenqi Lu, Yating Wan, Lin Zhang, Wenye Xu, Moses K. T. Li, Chengyu Liu, Chun Pan Cheung, Jessica Y. L. Ching, Pui Kuan Cheong, Ting Fan Leung, Sandra Chan, Patrick Leung, Francis K. L. Chan, Siew C. Ng","doi":"10.1038/s41564-024-01900-w","DOIUrl":"10.1038/s41564-024-01900-w","url":null,"abstract":"","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"10 2","pages":"600-600"},"PeriodicalIF":20.5,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41564-024-01900-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142763489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-02DOI: 10.1038/s41564-024-01857-w
Nazgul Sakenova, Elisabetta Cacace, Askarbek Orakov, Florian Huber, Vallo Varik, George Kritikos, Jan Michiels, Peer Bork, Pascale Cossart, Camille V. Goemans, Athanasios Typas
By acquiring or evolving resistance to one antibiotic, bacteria can become cross-resistant to a second antibiotic, which further limits therapeutic choices. In the opposite scenario, initial resistance leads to collateral sensitivity to a second antibiotic, which can inform cycling or combinatorial treatments. Despite their clinical relevance, our knowledge of both interactions is limited. We used published chemical genetics data of the Escherichia coli single-gene deletion library in 40 antibiotics and devised a metric that discriminates between known cross-resistance and collateral-sensitivity antibiotic interactions. Thereby we inferred 404 cases of cross-resistance and 267 of collateral-sensitivity, expanding the number of known interactions by over threefold. We further validated 64/70 inferred interactions using experimental evolution. By identifying mutants driving these interactions in chemical genetics, we demonstrated that a drug pair can exhibit both interactions depending on the resistance mechanism. Finally, we applied collateral-sensitive drug pairs in combination to reduce antibiotic-resistance development in vitro. Resistance to one antibiotic can make bacteria resistant or sensitive to another antibiotic, opening paths for combinatorial treatments. This study presents an approach to systematically discover and understand such antibiotic relationships.
{"title":"Systematic mapping of antibiotic cross-resistance and collateral sensitivity with chemical genetics","authors":"Nazgul Sakenova, Elisabetta Cacace, Askarbek Orakov, Florian Huber, Vallo Varik, George Kritikos, Jan Michiels, Peer Bork, Pascale Cossart, Camille V. Goemans, Athanasios Typas","doi":"10.1038/s41564-024-01857-w","DOIUrl":"10.1038/s41564-024-01857-w","url":null,"abstract":"By acquiring or evolving resistance to one antibiotic, bacteria can become cross-resistant to a second antibiotic, which further limits therapeutic choices. In the opposite scenario, initial resistance leads to collateral sensitivity to a second antibiotic, which can inform cycling or combinatorial treatments. Despite their clinical relevance, our knowledge of both interactions is limited. We used published chemical genetics data of the Escherichia coli single-gene deletion library in 40 antibiotics and devised a metric that discriminates between known cross-resistance and collateral-sensitivity antibiotic interactions. Thereby we inferred 404 cases of cross-resistance and 267 of collateral-sensitivity, expanding the number of known interactions by over threefold. We further validated 64/70 inferred interactions using experimental evolution. By identifying mutants driving these interactions in chemical genetics, we demonstrated that a drug pair can exhibit both interactions depending on the resistance mechanism. Finally, we applied collateral-sensitive drug pairs in combination to reduce antibiotic-resistance development in vitro. Resistance to one antibiotic can make bacteria resistant or sensitive to another antibiotic, opening paths for combinatorial treatments. This study presents an approach to systematically discover and understand such antibiotic relationships.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"10 1","pages":"202-216"},"PeriodicalIF":20.5,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41564-024-01857-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142758453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-02DOI: 10.1038/s41564-024-01885-6
Ilona I. Tosheva, Fabien Filaire, Willemijn F. Rijnink, Dennis de Meulder, Bianca van Kekem, Theo M. Bestebroer, Mathis Funk, Monique I. Spronken, C. Joaquin Cáceres, Daniel R. Perez, Mathilde Richard, Marion P. G. Koopmans, Pieter L. A. Fraaij, Ron A. M. Fouchier, Sander Herfst
An increase in spillover events of highly pathogenic avian influenza A(H5N1) viruses to mammals suggests selection of viruses that transmit well in mammals. Here we use air-sampling devices to continuously sample infectious influenza viruses expelled by experimentally infected ferrets. The resulting quantitative virus shedding kinetics data resembled ferret-to-ferret transmission studies and indicated that the absence of transmission observed for earlier A(H5N1) viruses was due to a lack of infectious virus shedding in the air, rather than the absence of necessary mammalian adaptation mutations. Whereas infectious human A(H1N1pdm) virus was efficiently shed in the air, infectious 2005 zoonotic and 2024 bovine A(H5N1) viruses were not detected in the air. By contrast, shedding of infectious virus was observed for 1 out of 4 ferrets infected with a 2022 European polecat A(H5N1) virus and a 2024 A(H5N1) virus isolated from a dairy farm worker. Spillover of avian A(H5N1) influenza virus to mammals may favour adaptation to these new hosts. Air sampling of infected ferrets shows that recent A(H5N1) strains, including one from a human case linked to the US cattle outbreak, are efficiently expelled into the air.
{"title":"Influenza A(H5N1) shedding in air corresponds to transmissibility in mammals","authors":"Ilona I. Tosheva, Fabien Filaire, Willemijn F. Rijnink, Dennis de Meulder, Bianca van Kekem, Theo M. Bestebroer, Mathis Funk, Monique I. Spronken, C. Joaquin Cáceres, Daniel R. Perez, Mathilde Richard, Marion P. G. Koopmans, Pieter L. A. Fraaij, Ron A. M. Fouchier, Sander Herfst","doi":"10.1038/s41564-024-01885-6","DOIUrl":"10.1038/s41564-024-01885-6","url":null,"abstract":"An increase in spillover events of highly pathogenic avian influenza A(H5N1) viruses to mammals suggests selection of viruses that transmit well in mammals. Here we use air-sampling devices to continuously sample infectious influenza viruses expelled by experimentally infected ferrets. The resulting quantitative virus shedding kinetics data resembled ferret-to-ferret transmission studies and indicated that the absence of transmission observed for earlier A(H5N1) viruses was due to a lack of infectious virus shedding in the air, rather than the absence of necessary mammalian adaptation mutations. Whereas infectious human A(H1N1pdm) virus was efficiently shed in the air, infectious 2005 zoonotic and 2024 bovine A(H5N1) viruses were not detected in the air. By contrast, shedding of infectious virus was observed for 1 out of 4 ferrets infected with a 2022 European polecat A(H5N1) virus and a 2024 A(H5N1) virus isolated from a dairy farm worker. Spillover of avian A(H5N1) influenza virus to mammals may favour adaptation to these new hosts. Air sampling of infected ferrets shows that recent A(H5N1) strains, including one from a human case linked to the US cattle outbreak, are efficiently expelled into the air.","PeriodicalId":18992,"journal":{"name":"Nature Microbiology","volume":"10 1","pages":"14-19"},"PeriodicalIF":20.5,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41564-024-01885-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142758452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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