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BJPsych Open. 2025 Apr 11;11(3):e86. doi: 10.1192/bjo.2025.32.

ABSTRACT

BACKGROUND: Rates of childhood mental health problems are increasing in the UK. Early identification of childhood mental health problems is challenging but critical to children's future psychosocial development. This is particularly important for children with social care contact because earlier identification can facilitate earlier intervention. Clinical prediction tools could improve these early intervention efforts.

AIMS: Characterise a novel cohort consisting of children in social care and develop effective machine learning models for prediction of childhood mental health problems.

METHOD: We used linked, de-identified data from the Secure Anonymised Information Linkage Databank to create a cohort of 26 820 children in Wales, UK, receiving social care services. Integrating health, social care and education data, we developed several machine learning models aimed at predicting childhood mental health problems. We assessed the performance, interpretability and fairness of these models.

RESULTS: Risk factors strongly associated with childhood mental health problems included age, substance misuse and being a looked after child. The best-performing model, a gradient boosting classifier, achieved an area under the receiver operating characteristic curve of 0.75 (95% CI 0.73-0.78). Assessments of algorithmic fairness showed potential biases within these models.

CONCLUSIONS: Machine learning performance on this prediction task was promising. Predictive performance in social care settings can be bolstered by linking diverse routinely collected data-sets, making available a range of heterogenous risk factors relating to clinical, social and environmental exposures.

PMID:40214105 | DOI:10.1192/bjo.2025.32

Eur J Cell Biol. 2025 Apr 4;104(2):151488. doi: 10.1016/j.ejcb.2025.151488. Online ahead of print.

ABSTRACT

Mitochondria adapt to the cell proliferative demands induced by growth factors through dynamic changes in morphology, distribution, and metabolic activity. Galectin-8 (Gal-8), a carbohydrate-binding protein that promotes cell proliferation by transactivating the EGFR-ERK signaling pathway, is overexpressed in several cancers. However, its impact on mitochondrial dynamics during cell proliferation remains unknown. Using MDCK and RPTEC kidney epithelial cells, we demonstrate that Gal-8 induces mitochondrial fragmentation and perinuclear redistribution. Additionally, mitochondria adopt donut-shaped morphologies, and live-cell imaging with two Keima-based reporters demonstrates Gal-8-induced mitophagy. ERK signaling inhibition abrogates all these Gal-8-induced mitochondrial changes and cell proliferation. Studies with established mutant versions of Gal-8 and CHO cells reveal that mitochondrial changes and proliferative response require interactions between the N-terminal carbohydrate recognition domain of Gal-8 and α-2,3-sialylated N-glycans at the cell surface. DRP1, a key regulator of mitochondrial fission, becomes phosphorylated in MDCK cells or overexpressed in RPTEC cells in an ERK-dependent manner, mediating mitochondrial fragmentation and perinuclear redistribution. Bafilomycin A abrogates Gal-8-induced cell proliferation, suggesting that mitophagy serves as an adaptation to cell proliferation demands. Functional analysis under Gal-8 stimulation shows that mitochondria maintain an active electron transport chain, partially uncoupled from ATP synthesis, and an increased membrane potential, indicative of healthy mitochondria. Meanwhile, the cells exhibit increased extracellular acidification rate and lactate production via aerobic glycolysis, a hallmark of an active proliferative state. Our findings integrate mitochondrial dynamics with metabolic adaptations during Gal-8-induced cell proliferation, with potential implications for physiology, disease, and therapeutic strategies.

PMID:40209344 | DOI:10.1016/j.ejcb.2025.151488

Nat Struct Mol Biol. 2025 Apr 9. doi: 10.1038/s41594-025-01530-8. Online ahead of print.

ABSTRACT

Pathogens have evolved diverse strategies to counteract host immunity. Ubiquitylation of lipopolysaccharide (LPS) on cytosol-invading bacteria by the E3 ligase RNF213 creates 'eat me' signals for antibacterial autophagy, but whether and how cytosol-adapted bacteria avoid LPS ubiquitylation remains poorly understood. Here, we show that the enterobacterium Shigella flexneri actively antagonizes LPS ubiquitylation through IpaH1.4, a secreted effector protein with ubiquitin E3 ligase activity. IpaH1.4 binds to RNF213, ubiquitylates it and targets it for proteasomal degradation, thus counteracting host-protective LPS ubiquitylation. To understand how IpaH1.4 recognizes RNF213, we determined the cryogenic electron microscopy structure of the IpaH1.4-RNF213 complex. The specificity of the interaction is achieved through the leucine-rich repeat of IpaH1.4, which binds the RING domain of RNF213 by hijacking the conserved RING interface required for binding to ubiquitin-charged E2 enzymes. IpaH1.4 also targets other E3 ligases involved in inflammation and immunity through binding to the E2-interacting face of their RING domains, including the E3 ligase LUBAC that is required for the synthesis of M1-linked ubiquitin chains on cytosol-invading bacteria downstream of RNF213. We conclude that IpaH1.4 has evolved to antagonize multiple antibacterial and proinflammatory host E3 ligases.

PMID:40205224 | DOI:10.1038/s41594-025-01530-8

Nat Microbiol. 2025 Apr 9. doi: 10.1038/s41564-025-02003-w. Online ahead of print.

NO ABSTRACT

PMID:40204877 | DOI:10.1038/s41564-025-02003-w

Proc Mach Learn Res. 2024 Jul;235:39529-39555.

ABSTRACT

Topological deep learning (TDL) is a rapidly evolving field that uses topological features to understand and design deep learning models. This paper posits that TDL is the new frontier for relational learning. TDL may complement graph representation learning and geometric deep learning by incorporating topological concepts, and can thus provide a natural choice for various machine learning settings. To this end, this paper discusses open problems in TDL, ranging from practical benefits to theoretical foundations. For each problem, it outlines potential solutions and future research opportunities. At the same time, this paper serves as an invitation to the scientific community to actively participate in TDL research to unlock the potential of this emerging field.

PMID:40196046 | PMC:PMC11973457

Sci Rep. 2025 Apr 7;15(1):11907. doi: 10.1038/s41598-025-95644-0.

ABSTRACT

The TMPRSS2 cell surface protease is used by a broad range of respiratory viruses to facilitate entry into target cells. Together with ACE2, TMPRSS2 represents a key factor for SARS-CoV-2 infection, as TMPRSS2 mediates cleavage of viral spike protein, enabling direct fusion of the viral envelope with the host cell membrane. Since the start of the COVID-19 pandemic, TMPRSS2 has gained attention as a therapeutic target for protease inhibitors which would inhibit SARS-CoV-2 infection, but little is known about TMPRSS2 regulation, particularly in cell types physiologically relevant for SARS-CoV-2 infection. Here, we performed an unbiased genome-wide CRISPR-Cas9 library screen, together with a library targeted at epigenetic modifiers and transcriptional regulators, to identify cellular factors that modulate cell surface expression of TMPRSS2 in human colon epithelial cells. We find that endogenous TMPRSS2 is regulated by the Elongin BC-VHL complex and HIF transcription factors. Depletion of Elongin B or treatment of cells with PHD inhibitors resulted in downregulation of TMPRSS2 and inhibition of SARS-CoV-2 infection. We show that TMPRSS2 is still utilised by SARS-CoV-2 Omicron variants for entry into colonic epithelial cells. Our study enhances our understanding of the regulation of endogenous surface TMPRSS2 in cells physiologically relevant to SARS-CoV-2 infection.

PMID:40195420 | PMC:PMC11976923 | DOI:10.1038/s41598-025-95644-0

J Virol. 2025 Apr 7:e0216724. doi: 10.1128/jvi.02167-24. Online ahead of print.

ABSTRACT

Synthesis of subgenomic RNAs is a strategy commonly used by polycistronic positive-sense single-stranded RNA viruses to express 3'-proximal genes. Members of the order Nidovirales, including coronaviruses and arteriviruses, use a unique discontinuous transcription strategy to synthesize subgenomic RNAs. In this study, in silico synonymous site conservation analysis and RNA structure folding predicted the existence of intra-family conserved high-order RNA structure within the M ORF of arteriviral genomes, which was further confirmed by RNA secondary structure probing. This RNA structure was determined to be important for the transcription/accumulation of subgenomic RNAs and the production of infectious viral particles. Mutations disrupting the stability of the RNA structures significantly decreased the accumulation of multiple subgenomic RNAs. In contrast, the impact of mutagenesis on full-length genomic RNA accumulation was limited. The degree to which wild-type levels of subgenomic RNA accumulation were maintained was found to correlate with the efficiency of infectious virus production. Moreover, the thermo-stability of stems within the high-order RNA structure is also well correlated with viral replication capacity and the maintenance of subgenomic RNA accumulation. This study is the first to report an intra-Arteriviridae conserved high-order RNA structure that is located in a protein-coding region and functions as an important cis-acting element to control the accumulation/transcription of arteriviral subgenomic RNAs. This work suggests a complex regulation mechanism between genome replication and discontinuous transcription in nidoviruses.IMPORTANCEArteriviruses are a group of RNA viruses that infect different animal species. They can cause diseases associated with respiratory/reproductive syndromes, abortion, or hemorrhagic fever. Among arteriviruses, porcine reproductive and respiratory syndrome virus (PRRSV) and equine arteritis virus (EAV) are economically important veterinary pathogens. The challenge in control of arterivirus infection reflects our limited knowledge of viral biology. In this study, we conducted a comprehensive analysis of arteriviral genomes and discovered intra-family conserved regions in the M ORF with a high-order RNA structure. The thermo-stability of the RNA structure influences sgRNA transcription/accumulation and correlates with the level of infectious virus production. Our studies provide new insight into arterivirus replication mechanisms, which may have implications for developing disease control and prevention strategies.

PMID:40192289 | DOI:10.1128/jvi.02167-24

Front Vet Sci. 2025 Mar 19;12:1551065. doi: 10.3389/fvets.2025.1551065. eCollection 2025.

ABSTRACT

Bovine tuberculosis (bTB) severely impacts Ethiopia's growing dairy sector, where test-and-cull control methods are economically unfeasible, and test-and-segregation is impractical in herds with very high prevalence. We assessed the feasibility of establishing bTB-free replacement stock through early segregation of calves born to bTB-positive cows. In a two-year longitudinal study on a high-prevalence (98% tuberculin skin test positive) dairy farm, 26 newborn calves were separated from their bTB-positive dams on day five after birth and screened for bTB at 2 to 5 month intervals across eight rounds, with test-positive calves immediately removed from the negative herd. The majority of segregated calves (19 out of 25; 76%; 95% CI: 58-94) remained bTB-test negative through the testing period, with nine uninfected female calves and two males reaching 18 months of age, demonstrating potential for establishing bTB-free breeding stock. However, six calves (24%; 95% CI: 6-42) turned to test positive during the study period. The extended dam-calf contact during the first five days likely contributed to some infections, suggesting that immediate separation and alternative colostrum sources could improve success rates. The addition of interferon gamma release assays in later testing rounds enabled detection of infected animals potentially missed by skin testing alone, highlighting the value of complementary diagnostic approaches for surveillance. These findings provide preliminary evidence that early calf segregation can generate bTB-negative replacement stock from infected herds, and provide a framework for larger-scale studies across different farm settings.

PMID:40177672 | PMC:PMC11963379 | DOI:10.3389/fvets.2025.1551065

Nat Methods. 2025 Apr;22(4):641-645. doi: 10.1038/s41592-025-02635-0.

NO ABSTRACT

PMID:40175561 | DOI:10.1038/s41592-025-02635-0

Am J Infect Control. 2025 Apr 2:S0196-6553(25)00127-0. doi: 10.1016/j.ajic.2025.03.014. Online ahead of print.

NO ABSTRACT

PMID:40172504 | DOI:10.1016/j.ajic.2025.03.014

Biomed Pharmacother. 2025 Mar 31;186:117957. doi: 10.1016/j.biopha.2025.117957. Online ahead of print.

ABSTRACT

BACKGROUND: Overactive neutrophilic inflammation causes damage to the airways and death in people with cystic fibrosis (CF), a genetic disorder resulting from mutations in the CFTR gene. Reducing the impact of inflammation is therefore a major concern in CF. Evidence indicates that dysfunctional NRF2 signaling in CF individuals may impair their ability to regulate their oxidative and inflammatory responses, although the role of NRF2 in neutrophil-dominated inflammation and tissue damage associated with CF has not been determined. Therefore, we examined whether curcumin, an activator of NRF2, might provide a beneficial effect in the context of CF.

METHODS: Combining Cftr-depleted zebrafish as an innovative biomedical model with CF patient-derived airway organoids (AOs), we aimed to understand how NRF2 dysfunction leads to abnormal inflammatory status and tissue remodeling and determine the effects of curcumin in reducing inflammation and tissue damage in CF.

RESULTS: We demonstrate that NFR2 is instrumental in regulating neutrophilic inflammation and repair processes in vivo, thereby preventing inflammatory damage. Importantly, curcumin treatment restores NRF2 activity in both CF zebrafish and AOs. Curcumin reduces neutrophilic inflammation in CF context, by rebalancing the production of epithelial ROS and pro-inflammatory cytokines. Furthermore, curcumin improves tissue repair by reducing CF-associated fibrosis. Our findings demonstrate that curcumin prevents CF-mediated inflammation via activating the NRF2 pathway.

CONCLUSIONS: This work highlights the protective role of NRF2 in limiting inflammation and injury and show that therapeutic strategies to normalize NRF2 activity, using curcumin or others NRF2 activators, might simultaneously reduce airway inflammation and damage in CF.

PMID:40168724 | DOI:10.1016/j.biopha.2025.117957

Microb Genom. 2025 Mar;11(3). doi: 10.1099/mgen.0.001366.

ABSTRACT

Streptococcus equi subsp. equi causes the equine respiratory disease 'strangles', which is highly contagious, debilitating and costly to the equine industry. S. equi emerged from the ancestral Streptococcus equi subsp. zooepidemicus and continues to evolve and disseminate globally. Previous work has shown that there was a global population replacement around the beginning of the twentieth century, obscuring the early genetic events in this emergence. Here, we have used large-scale genomic analysis of S. equi and its ancestor S. zooepidemicus to identify evolutionary events, leading to the successful expansion of S. equi. One thousand two hundred one whole-genome sequences of S. equi were recovered from clinical samples or from data available in public databases. Seventy-four whole-genome sequences representative of the diversity of S. zooepidemicus were used to compare the gene content and examine the evolutionary emergence of S. equi. A dated Bayesian phylogeny was constructed, and ancestral state reconstruction was used to determine the order and timing of gene gain and loss events between the different species and between different S. equi lineages. Additionally, a newly developed framework was used to investigate the fitness of different S. equi lineages. We identified a novel S. equi lineage, comprising isolates from donkeys in Chinese farms, which diverged nearly 300 years ago, after the emergence of S. equi from S. zooepidemicus, but before the global sweep. Ancestral state reconstruction demonstrated that phage-encoded virulence factors slaA, seeL and seeM were acquired by the global S. equi after the divergence of the basal donkey lineage. We identified the equibactin locus in both S. equi populations, but not S. zooepidemicus, reinforcing its role as a key S. equi virulence mechanism involved in its initial emergence. Evidence of a further population sweep beginning in the early 2000s was detected in the UK. This clade now accounts for more than 80% of identified UK cases since 2016. Several sub-lineages demonstrated increased fitness, within which we identified the acquisition of a new, fifth prophage containing additional toxin genes. We definitively show that acquisition of the equibactin locus was a major determinant in S. equi becoming an equid-exclusive pathogen, but that other virulence factors were fixed by the population sweep at the beginning of the twentieth century. Evidence of a secondary population sweep in the UK and acquisition of further advantageous genes implies that S. equi is continuing to adapt, and therefore, continued investigations are required to determine further risks to the equine industry.

PMID:40152912 | DOI:10.1099/mgen.0.001366

Nat Microbiol. 2025 Apr;10(4):813-816. doi: 10.1038/s41564-025-01969-x.

NO ABSTRACT

PMID:40140704 | DOI:10.1038/s41564-025-01969-x

Curr Biol. 2025 Apr 7;35(7):1549-1561.e3. doi: 10.1016/j.cub.2025.02.044. Epub 2025 Mar 21.

ABSTRACT

Adaptive mechanisms in bacteria, which are widely assumed to be haploid or partially diploid, are thought to rely on the emergence of spontaneous mutations or lateral gene transfer from a reservoir of pre-existing variants within the surrounding environment. These variants then become fixed in the population upon exposure to selective pressures. Here, we show that multiple distinct wild-type (WT) substrains of the highly polyploid cyanobacterium Synechocystis sp. PCC 6803 can adapt rapidly to the potent herbicide methyl viologen (MV). Genome sequencing revealed that the mutations responsible for adaptation to MV were already present prior to selection in the genomes of the unadapted parental strains at low allelic frequencies. This indicates that chromosomal polyploidy in bacteria can provide cells with a reservoir of conditionally beneficial mutations that can become rapidly enriched and fixed upon selection. MV-resistant strains performed oxygenic photosynthesis less efficiently than WTs when MV was absent, suggesting trade-offs in cellular fitness associated with the evolution of MV resistance and a possible role for balancing selection in the maintenance of these alleles under ecologically relevant growth conditions. Resistance was associated with reduced intracellular accumulation of MV. Our results indicate that genome polyploidy plays a role in the rapid adaptation of some bacteria to stressful conditions, which may include xenobiotics, nutrient limitation, environmental stresses, and seasonal changes.

PMID:40120581 | DOI:10.1016/j.cub.2025.02.044

Proc Natl Acad Sci U S A. 2025 Mar 25;122(12):e2502064122. doi: 10.1073/pnas.2502064122. Epub 2025 Mar 20.

ABSTRACT

West Nile virus (WNV) and Usutu virus (USUV) are closely related mosquito-borne neurotropic flaviviruses that share common transmission cycle and can infect humans. However, while human infections by WNV are widespread, infections by USUV are comparatively less frequent, less severe, and currently limited to Africa and Europe. To identify human host factors that contribute to the pathogenic signatures of these two flaviviruses, we carried out an arrayed expression screen of over 1,300 interferon-stimulated genes (ISGs). Several ISGs known to target flaviviruses, including IFI6, SHFL, and RTP4 were among the strongest hits. Interestingly, we also found MITD1, an ISG with no previously reported antiviral activity, among the strongest hits. We demonstrated that the antiviral activity of MITD1 was not limited to USUV and WNV, since it also inhibited Zika and dengue virus replication. We found MITD1 to interfere with viral RNA replication by sequestering specific endosomal sorting complexes required for transport-III (ESCRT-III) proteins involved in the formation of viral replication factories. MITD1 expression was not increased by type I interferon (IFN-I) in most human cells and mouse tissues that we examined, although WNV and USUV replication was strongly inhibited by IFN-I. Strikingly, MITD1 was induced in the brain of USUV-infected mice and importantly, in human monocyte-derived microglia. Using human microglial-like cells, we confirmed that MITD1 is an essential mediator of the anti-flavivirus activity of IFN-I in these cells. We conclude that MITD1 plays a key role in the cellular defenses against neurotropic flaviviruses.

PMID:40112111 | PMC:PMC11962514 | DOI:10.1073/pnas.2502064122

mBio. 2025 Apr 9;16(4):e0032225. doi: 10.1128/mbio.00322-25. Epub 2025 Mar 14.

ABSTRACT

Mycobacterium abscessus is one of the leading causes of pulmonary infections caused by non-tuberculous mycobacteria. The ability of M. abscessus to establish a chronic infection in the lung relies on a series of adaptive mutations impacting, in part, global regulators and cell envelope biosynthetic enzymes. One of the genes under strong evolutionary pressure during host adaptation is ubiA, which participates in the elaboration of the arabinan domains of two major cell envelope polysaccharides: arabinogalactan (AG) and lipoarabinomannan (LAM). We here show that patient-derived UbiA mutations not only cause alterations in the AG, LAM, and mycolic acid contents of M. abscessus but also tend to render the bacterium more prone to forming biofilms while evading uptake by innate immune cells and enhancing their pro-inflammatory properties. The fact that the effects of UbiA mutations on the physiology and pathogenicity of M. abscessus were impacted by the rough or smooth morphotype of the strain suggests that the timing of their selection relative to morphotype switching may be key to their ability to promote chronic persistence in the host.IMPORTANCEMultidrug-resistant pulmonary infections caused by Mycobacterium abscessus and subspecies are increasing in the U.S.A. and globally. Little is known of the mechanisms of pathogenicity of these microorganisms. We have identified single-nucleotide polymorphisms (SNPs) in a gene involved in the biosynthesis of two major cell envelope polysaccharides, arabinogalactan and lipoarabinomannan, in lung-adapted isolates from 13 patients. Introduction of these individual SNPs in a reference M. abscessus strain allowed us to study their impact on the physiology of the bacterium and its interactions with immune cells. The significance of our work is in identifying some of the mechanisms used by M. abscessus to colonize and persist in the human lung, which will facilitate the early detection of potentially more virulent clinical isolates and lead to new therapeutic strategies. Our findings may further have broader biomedical impacts, as the ubiA gene is conserved in other tuberculous and non-tuberculous mycobacterial pathogens.

PMID:40084888 | PMC:PMC11980365 | DOI:10.1128/mbio.00322-25

Bioinformatics. 2025 Mar 4;41(3):btaf103. doi: 10.1093/bioinformatics/btaf103.

ABSTRACT

MOTIVATION: Computational models are crucial for addressing critical questions about systems evolution and deciphering system connections. The pivotal feature of making this concept recognizable from the biological and clinical community is the possibility of quickly inspecting the whole system, bearing in mind the different granularity levels of its components. This holistic view of system behaviour expands the evolution study by identifying the heterogeneous behaviours applicable, e.g. to the cancer evolution study.

RESULTS: To address this aspect, we propose a new modelling paradigm, UnifiedGreatMod, which allows modellers to integrate fine-grained and coarse-grained biological information into a unique model. It enables functional studies by combining the analysis of the system's multi-level stable states with its fluctuating conditions. This approach helps to investigate the functional relationships and dependencies among biological entities. This is achieved, thanks to the hybridization of two analysis approaches that capture a system's different granularity levels. The proposed paradigm was then implemented into the open-source, general modelling framework GreatMod, in which a graphical meta-formalism is exploited to simplify the model creation phase and R languages to define user-defined analysis workflows. The proposal's effectiveness was demonstrated by mechanistically simulating the metabolic output of Escherichia coli under environmental nutrient perturbations and integrating a gene expression dataset. Additionally, the UnifiedGreatMod was used to examine the responses of luminal epithelial cells to Clostridium difficile infection.

AVAILABILITY AND IMPLEMENTATION: GreatMod https://qbioturin.github.io/epimod/, epimod_FBAfunctions https://github.com/qBioTurin/epimod_FBAfunctions, first case study E. coli https://github.com/qBioTurin/Ec_coli_modelling, second case study C. difficile https://github.com/qBioTurin/EpiCell_CDifficile.

PMID:40073274 | PMC:PMC11932724 | DOI:10.1093/bioinformatics/btaf103

Am J Respir Crit Care Med. 2025 Mar 12. doi: 10.1164/rccm.202409-1824OC. Online ahead of print.

ABSTRACT

RATIONALE: Mycobacterium abscessus group bacteria (MABS) cause lethal infections in people with chronic lung diseases. Transmission mechanisms remain poorly understood; the detection of dominant circulating clones (DCCs) has suggested potential for person-to-person transmission.

OBJECTIVES: This study aimed to determine the role of drinking water in the transmission of MABS.

METHODS: A total of 289 isolates were cultured from respiratory samples (231) and drinking water sources (58) across Queensland, Australia.

MEASUREMENTS AND MAIN RESULTS: Whole genome sequences were analysed to identify DCCs and determine relatedness. Half of the isolates (144, 49·8%) clustered with previously described DCCs, of which 30 formed a clade within DCC5. Pangenomic analysis of the water-associated DCC5 clade revealed an enrichment of genes associated with copper resistance. Four instances of plausible epidemiological links were identified between genomically-related clinical and water isolates.

CONCLUSIONS: We provide evidence that drinking water is a reservoir for MABS and may be a vector in the chain of MABS infection.

PMID:40072241 | DOI:10.1164/rccm.202409-1824OC

This Cambridge Immunology and Medicine Seminar will take place on Thursday 29 May 2025, starting at 4:00pm, in the Ground Floor Lecture Theatre, Jeffrey Cheah Biomedical Centre (JCBC)

Speaker: Prof. Jonathan W Yewdell, Senior Investigator Cellular Biology Cellular Biology and Viral Immunology Section, The National Institute of Allergy and Infectious Diseases (NIAID)

Title: TBC

Host: Prof. Louise Boyle, Department of Pathology, Cambridge

Refreshments will be available following the seminar.

• Speaker: Prof. Jonathan W Yewdell, Senior Investigator Cellular Biology Cellular Biology and Viral Immunology Section, The National Institute of Allergy and Infectious Diseases (NIAID)
• Thursday 15 May 2025, 16:00-17:00
• Venue: Lecture Theatre, Jeffrey Cheah Biomedical Centre, Cambridge Biomedical Campus.
• Series: Cambridge Immunology Network Seminar Series; organiser: Ruth Paton.

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Wellcome Open Res. 2025 Jan 13;10:5. doi: 10.12688/wellcomeopenres.23494.1. eCollection 2025.

ABSTRACT

The increasing threat from infection with drug-resistant pathogens is among the most serious public health challenges of our time. Formed by Wellcome in 2018, the Surveillance and Epidemiology of Drug-Resistant Infections Consortium (SEDRIC) is an international think tank whose aim is to inform policy and change the way countries track, share, and analyse data relating to drug-resistant infections, by defining knowledge gaps and identifying barriers to the delivery of global surveillance. SEDRIC delivers its aims through discussions and analyses by world-leading scientists that result in recommendations and advocacy to Wellcome and others. As a result, SEDRIC has made key contributions in furthering global and national actions. Here, we look back at the work of the consortium between 2018-2024, highlighting notable successes. We provide specific examples where technical analyses and recommendations have helped to inform policy and funding priorities that will have real-world impact on the surveillance and epidemiology of infections with drug-resistant pathogens.

PMID:40062317 | PMC:PMC11885901 | DOI:10.12688/wellcomeopenres.23494.1