Objective The study aims to investigate the prevalence of extended-spectrum β-lactamase (ESBL) genes (blaCTX-M-1, blaTEM, blaSHV) in Klebsiella pneumoniae (K. pneumoniae) and Escherichia coli (E. coli) isolates recovered from hospital environmental swab samples, including bed surfaces, floors, and waste bins, in Northeastern Bangladesh. Method A total of 54 samples were randomly collected from hospital wards. Isolates were identified using cultural and biochemical tests and tested for β-lactam susceptibility. ESBL and other resistance genes (tetB, gyrA) were detected by molecular analysis. Results Among 62 phenotypically resistant isolates (39 K. pneumoniae, 23 E. coli), 74% of K. pneumoniae and 91% of E. coli harbored the blaCTX-M-1 gene, 73% and 91% carried the blaTEM gene, and 18% and 5% carried the blaSHV gene, respectively. Additionally, 5% of K. pneumoniae and 27% of E. coli possessed the tetB gene, while 22% and 95% carried the gyrA gene. Phylogenetic analysis confirmed clustering of blaSHV, blaCTX-M-1, and blaTEM genes within their respective families. Multidrug resistance was observed in 90% of isolates, with E. coli at 95% and K. pneumoniae at 87%. Furthermore, 7.5% of K. pneumoniae and 17.4% of E. coli exhibited pan-resistance to seven antibiotic classes. Conclusion The results highlight the urgent need to address the antimicrobial resistance crisis in hospital settings to reduce the risk of nosocomial infections in Bangladesh.
Background Oncogenic intracellular bacteria, including Chlamydia trachomatis, Mycoplasma genitalium, and Fusobacterium nucleatum, have emerged as significant contributors to cervical carcinogenesis. Despite growing interest in microbial oncology, the molecular epidemiological landscape and phylogeographic distribution of these pathogens in Northern China remain poorly characterized. This study aimed to determine the prevalence, co-infection patterns, genotypic diversity, and spatial phylogeographic clustering of oncogenic intracellular bacteria among cervical cancer patients across five provinces of Northern China. Methods A cross-sectional, multi-center study was conducted between March 2022 and November 2024 across Shaanxi, Heilongjiang, Beijing, Shandong, and Inner Mongolia. Cervical swab specimens were collected from 1247 confirmed cervical cancer patients. Pathogen detection was performed using multiplex real-time polymerase chain reaction, 16S rRNA gene amplicon sequencing, and whole-genome sequencing. Phylogeographic analyses employed maximum likelihood and Bayesian evolutionary inference frameworks. Statistical analyses included multivariate logistic regression and geographic information system-based spatial clustering. Results The overall prevalence of at least one oncogenic intracellular bacterium was 68.3% (n = 852). Chlamydia trachomatis was the most prevalent pathogen detected in 41.2% of participants. Co-infection with two or more bacteria was identified in 29.7% of cases and was independently associated with advanced-stage cervical cancer (adjusted odds ratio = 2.87; 95% confidence interval: 1.94 to 4.23; p < 0.001). Phylogeographic analysis revealed three distinct molecular clades with evidence of bidirectional gene flow between Shaanxi and Heilongjiang. Whole-genome sequencing identified 14 novel virulence gene variants not previously characterized in Chinese clinical isolates. Conclusions Oncogenic intracellular bacteria are highly prevalent and genotypically diverse among cervical cancer patients in Northern China. The identified phylogeographic clustering and novel virulence variants have direct implications for regional screening programs, targeted antimicrobial strategies, and the development of region-specific molecular diagnostic panels.
INTRODUCTION:The human leukocyte antigen G (HLA-G) allele repertoire is crucial for cell-mediated immune responses. While HLA-G's role in human papillomavirus (HPV) infection is increasingly studied, research on HLA-G and humoral immunity remains limited. This study aimed to establish whether HLA-G alleles impact type-specific HPV serological outcomes. METHODS:Altogether, 265 women from the prospective Finnish Family HPV cohort study were included. HLA-G alleles and genotypes were determined by direct DNA-sequencing. Blood samples were collected at baseline (36 weeks of pregnancy) and at 12, 24 and 36 months of follow-up. Antibodies to the L1 antigen of HPV types 6, 11, 16, 18 and 45 were determined using multiplex serology. RESULTS*: Six different HLA-G alleles and genotypes were identified. The most common allele was 01:01:01 (87.2%) followed by *01:01:02 (39.6%). Heterozygote carriage of HLA-G*01:01:01 increased the likelihood of HPV16 seropersistence (OR 2.99; 95%CI 1.13-7.91). Allele *01:01:03 was associated with both increased HPV11 seropositivity (OR 3.93; 95%CI 1.49-10.39) and seropersistence (OR 4.42; 95%CI 1.56-12.49). Conversely, allele *01:04:01 showed a protective association against HPV11 seropositivity (OR 0.43, 95%CI 0.20-0.91). CONCLUSIONS:HLA-G alleles and genotypes may influence seropositivity and seropersistence to L1 antigen of both low-risk HPV11 and high-risk HPV16 genotypes. Given study limitations, these findings should be considered exploratory, and further research is warranted to establish the detailed mechanisms by which HLA-G influences HPV-related humoral immunity and disease outcomes.
Pseudomonas aeruginosa is a major opportunistic pathogen and a leading cause of nosocomial infections in the Asia-Pacific region. This comparative genomic case study investigated 18 P. aeruginosa isolates, categorized into nine ST-matched sets to minimize phylogenetic noise and identify genomic divergence between clinical and environmental habitats. The isolates represent both globally distributed high-risk clones (ST235, ST357, ST308) and sporadic lineages (ST274, ST316, ST381). The genomes possessed a mean size of 6.7 ± 0.2 Mbp and shared a core genome of 4639 genes. Virulence profiling revealed a strictly mutually exclusive distribution of exoU (cytotoxic) and exoS (invasive) genotypes. While exoU was detected in both clinical and environmental isolates, the spcU chaperone gene was entirely absent in the environmental group. Even among clinical exoU-positive isolates, spcU was only present in 42.8% (3/7) of the strains, indicating that the complete exoU-spcU locus is not consistently maintained in either setting. Clinical isolates generally harbored a higher density of acquired antimicrobial resistance genes (ARGs), including determinants such as qnrVC1 and blaVEB-9, whereas the blaNDM-1 carbapenemase and chromosomal mutations (gyrA T83I; basR L71R) were maintained across both ecological sources. Mobile genetic elements (MGEs) were the primary drivers of accessory genome divergence, with high-risk lineages exhibiting a robust resistance backbone regardless of their origin. As a targeted, hypothesis-generating case study without formal statistical testing, these results are consistent with lineage-specific genomic divergence rather than a confirmed species-wide evolutionary transition. Our findings underscore that environmental reservoir in the Asia-Pacific harbor high-risk clones with significant resistance potential, necessitating sustained regional genomic surveillance across diverse habitats.
OBJECTIVE:To investigate the association and potential mechanisms between H7N9 influenza virus infection or vaccination and immune thrombocytopenia (ITP), providing foundational data for the prevention and treatment of related ITP. METHODS:Using laboratory-prepared anti-H7N9 influenza virus monoclonal antibodies (mAbs) (H7N9-98 and H7N9-120) as research subjects, the interactions between these antibodies and human platelets were analyzed through Western blotting (WB), immunohistochemistry (IHC), and immunofluorescence (IF) techniques. RESULTS:The mAb H7N9-98 exhibited specific binding to human platelets, showing positive results in both IHC and IF assays. Western blotting results demonstrated that this antibody could specifically recognize approximately 60 kDa human platelet proteins. The isotype control mAb H7N9-120 did not exhibit the aforementioned binding reactions, with all test results being negative. CONCLUSION:These findings suggest that the specific antibodies induced by the H7N9 virus may mediate platelet damage through cross-reactivity with platelet autoantigens. This mechanism warrants further investigation to provide experimental evidence for the pathogenesis of secondary ITP associated with H7N9 infection.
Mycobacterium abscessus is a nontuberculous mycobacterium recognized as an emerging opportunistic pathogen that poses a growing clinical challenge worldwide. It causes recalcitrant pulmonary and extrapulmonary infections and is characterized by morphotype switching and biofilm-forming capacity. These phenotypic features are considered important virulence determinants; however, the genetic factors underlying phenotypic variability remain poorly understood. The biofilm-forming capacity, mutations associated with morphotype variation, and genetic determinants linked to deficient biofilm formation were investigated in 58 clinical Mycobacterium abscessus isolates recovered from non-cystic fibrosis patients. For biofilm-forming capability, 41.4% (n = 24) of isolates were categorized as strong producers, 51.7% (n = 30) as moderate producers, and 6.9% (n = 4) as weak producers. Smooth morphotype isolates produced significantly greater biofilm biomass than rough isolates (p = 0.006). Genomic analysis demonstrated that the rough morphotype was significantly associated with genetic alterations, including point mutations, insertions/deletions (indels), and large genomic deletions disrupting genes involved in glycopeptidolipid (GPL) biosynthesis, particularly mps1 and mps2. Longitudinal analysis of serial isolates obtained from a single patient revealed a massive 37.6-kb deletion and loss-of-function mutations in genes associated with stress response (lat), metabolism (atsA), and membrane transport (mspA) among weak biofilm-forming isolates. Notably, the mutations potentially contributing to morphotype switching and altered biofilm-forming capacity occur spontaneously across these clinical isolates. Collectively, these findings identify genomic determinants associated with morphotype transition and biofilm attenuation in M. abscessus, highlighting potential targets for strategies aimed at disrupting biofilm formation and improving the management of M. abscessus infections.
In this study, we selected Acinetobacter baumannii Ab2897, a strain from our laboratory, as the host, while the lytic bacteriophage vB_AbaP_IME546 was isolated from untreated hospital sewage. We examined the phage's biological characteristics and found that its latent period was under 5 min, with complete lysis of the bacteria occurring within 60 min. The plaques formed by the bacteriophage showed a halo, indicating the presence of an antibacterial protein. Consequently, this phage underwent next-generation sequencing. A BLAST analysis of the assembled genome sequence indicated that vB_AbaP_IME546 is a novel bacteriophage. After carrying out RAST annotation, it was proposed that the tail fiber protein of the bacteriophage might possess depolymerase activity. To further explore this, the ORF49 gene encoding the tail fiber protein was cloned and expressed. The resulting protein, Dp49, was successfully generated. When the protein was applied to a double-layer plate assay, a transparent halo formed in the area surrounding the bacterial growth. This finding confirms that the IME546 phage exhibits depolymerase activity during the lysis of Ab2897.
Colorectal cancer (CRC) is a multifactorial disease influenced by genetic, environmental, and microbial factors. Within the gut microbiota, pks + Escherichia coli has emerged as a key contributor to colorectal carcinogenesis through the production of colibactin, a genotoxic secondary metabolite. Colibactin induces DNA damage by forming interstrand crosslinks and promoting replication-associated double-strand breaks, thereby triggering host DNA damage response pathways and genomic instability. Recent advances in genomic profiling have identified distinct mutational signatures, such as SBS88 and ID18, in colorectal tumors, providing molecular evidence of prior colibactin exposure. Notably, emerging data suggest that these signatures are enriched in early-onset CRC, highlighting a potential role for bacterial genotoxins in tumor initiation at younger ages. In parallel, inflammation, dysbiosis and interactions with the tumor microenvironment may further modulate disease progression. In addition to mechanistic insights, growing attention has focused on translational applications, including the use of microbial markers, exosomes, and miRNA profiles as potential diagnostic and prognostic tools. However, significant challenges remain, including the high prevalence of pks + E. coli among healthy individuals, population variability, and the difficulty of establishing causality from associative data. This review summarizes current evidence on the role of colibactin-producing bacteria in CRC pathogenesis, integrates recent genomic findings, and discusses emerging diagnostic and therapeutic perspectives, while highlighting key limitations and future research directions.
OBJECTIVES:Enterobacter hormaechei is an opportunistic pathogen increasingly implicated in healthcare-associated infections, including bloodstream infections. However, the genomic and pathogenic features of clinical isolates from specific surgical settings remain incompletely characterized. METHODS:We performed whole-genome sequencing and comprehensive genomic analysis of a clinical E. hormaechei isolate (strain FLZ) recovered from a patient who developed fatal septic shock following left atrial myxoma resection. Antimicrobial resistance genes and virulence factors were identified using curated databases with stringent thresholds. The in vivo virulence of FLZ was assessed using a murine peritonitis model. RESULTS:The FLZ genome comprised 4,609,213 bp with a GC content of 55.3%, encoding 4377 predicted genes. Phylogenomic analysis confirmed its classification as E.hormaechei subsp. xiangfangensis (99.09% ANI with the type strain). The isolate carried resistance-associated genes and efflux pump components. Virulence gene profiling identified 61 curated virulence-associated genes, most notably the complete enterobactin biosynthesis and uptake system. At the intermediate infection dose of 108 CFU/mL, the FLZ strain demonstrated significantly higher pathogenicity compared to the reference strain, with a median survival time of 3.3 days (95% Confidence Interval: 0.5-6.1) compared to 8.7 days for the reference strain (P = 0.02, 95% Confidence Interval: 6.3-11.1). CONCLUSION:This study provides genomic and in vivo evidence characterizing the pathogenic potential of an E. hormaechei clinical isolate from a rare postoperative setting. The findings highlight the need for enhanced surveillance and further functional studies to elucidate the virulence mechanisms of this emerging pathogen.
Whole-genome sequencing (WGS) provides high-resolution insight into the genetic diversity, transmission dynamics, and drug-resistance mechanisms of Mycobacterium tuberculosis (MTB), yet genomic data from Morocco remain limited. In this study, we analyzed 68 WGS datasets of Moroccan MTB isolates and contextualized them using 19 global reference genomes. Lineages and resistance-associated mutations were determined with TB-Profiler. Pairwise single-nucleotide polymorphism (SNP) distances, phylogeny and transmission clusters were defined using well-established SNP thresholds implemented in the MTBseq pipeline. In silico spoligotypes were further compared with the SITVITEXTEND database to place Moroccan isolates in a broader regional context. Results demonstrated that circulating MTB strains in Morocco were dominated by Euro-American Lineage 4 (89.7%), with a smaller contribution from the Beijing lineage (L2.2.1). Resistance to rifampicin and isoniazid was mainly driven by canonical rpoB Ser450Leu and katG Ser315Thr mutations, while resistance to other drugs involved diverse variants. Seventeen genomic clusters encompassing 73.5% of isolates were identified, including nine clusters with isolates differing by 0-5 SNPs, consistent with very recent transmission. Multidrug-resistant and pre-extensively drug-resistant isolates were disproportionately concentrated within LAM 4.3 and Beijing sub-lineages. Spoligotyping comparisons confirmed the predominance of Euro-American lineages across Morocco and neighboring Mediterranean countries. This first comprehensive WGS-based analysis provides crucial insights into the molecular epidemiology of tuberculosis in Morocco, emphasizing the importance of integrating genomic tools into national TB control programs. Understanding the genetic landscape and transmission pathways of M. tuberculosis will support more effective public health strategies aimed at reducing TB incidence and preventing the spread of drug-resistant strains.
Zoonotic spillover, the transmission of pathogens between animals and humans, is increasingly recognized as a major driver of emerging infectious diseases. However, most spillover research continues to approach emergence as a pathogen-specific or event-based phenomenon, limiting the ability to generalize findings across biological systems or to anticipate emergence before outbreaks occur. In this review, we build upon the existing eco-evolutionary framework to develop a pathogen-agnostic conceptual and operational framework that positions spillover as an emergent outcome of interacting ecological and evolutionary processes operating across hosts, environments, and time. The framework is organized around four interacting system-level pillars: pathogen evolvability, host network architecture, environmental mediation of persistence and exposure, and selective filtering and amplification under ecological and anthropogenic change. We propose that spillover risk emerges nonlinearly from the convergence of these interacting processes rather than from any single factor acting independently. Importantly, we move beyond conceptual synthesis by outlining measurable indicators and empirically testable approaches derived from genomics, ecology, environmental surveillance, and network analysis to operationalize the framework across diverse pathogen systems. Additionally, we discuss comparative and longitudinal study designs to evaluate spillover dynamics among viruses, bacteria, parasites, and other microbial threats. By reframing spillover as a dynamic eco-evolutionary system rather than an isolated transmission event, this review provides a comparative and operational foundation for studying zoonotic emergence and for informing surveillance, early warning, and intervention strategies amid accelerating environmental changes.
BACKGROUND:Since the beginning of the COVID-19 pandemic, a large number of SARS-CoV-2 variants have emerged from the reference strain (Wuhan-Hu-1, NC_045512.2). Using these variants to understand the genetic diversity and temporal dynamics of SARS-CoV-2 in Niger is essential for developing and implementing effective public health interventions. METHOD:SARS-CoV-2 detection was performed on nasopharyngeal samples collected from travelers and symptomatic patients at the National Reference Laboratory in Niger from March 2020 to March 2023 using RT-qPCR techniques. A subset of samples with a cycle threshold <28 were selected for whole-genome sequencing and genomic analysis, which included phylogenetic reconstruction to study the evolutionary relationships of SARS-CoV-2 variants detected in Niger. RESULTS:Among 286,872 samples from suspected cases tested, we confirmed 8266 positives for SARS-CoV-2, resulting in a positivity rate of 2.88%. Of the positive cases, 268 (3.24%) resulted in death and 5577 (67.48%) were travelers. All the WHO-designated Variants of Concern (VOCs), including Alpha B.1.1.7 (n = 2), Beta B.1.351 (n = 1), Delta B.1.617 (n = 20) and Omicron B.1.1.529 (n = 95) circulated in Niger during the study period. Among the Variants of Interest (VOIs) and Variants Under Monitoring (VUMs), the A27 lineage (n = 49) was the predominant virus detected and co-circulated with Eta lineage B.1.525 (n = 21). Phylogeographic analysis identified at least 60 independent introductions of SARS-CoV-2 into Niger, the majority of which were closely related to published sequences from other African countries (n = 25) and European countries (n = 24). Phylogenetic analysis of the four predominant variants revealed a temporal progression of SARS-CoV-2 lineages in Niger, with well-supported clades. A high number of mutations were observed, mainly located in the spike protein, ORF1a, and ORF1b genes. CONCLUSION:This study helps to understand the SARS-CoV-2 evolution and dynamics in Niger Republic, where diagnostic capacities and containment measures were challenging.
BACKGROUND:Escherichia coli poses a global health threat from increasing β-lactam resistance. This study uses genomic and One Health data to map resistance patterns and enhance antimicrobial resistance (AMR) prediction and management. METHODS:This study performed a One Health whole-genome analysis of 30,554 E. coli isolates from human, animal, and environmental sources, collected between 2000 and 2025. Publicly available genomic data were retrieved from NCBI, encompassing β-lactam resistance genes, encoding extended-spectrum β-lactamases, AmpC, and carbapenemases, along with key chromosomal resistance-associated mutations. Resistance determinants were identified and curated using AMRFinderPlus. Multilocus sequence typing (MLST) and pathotype assignments were conducted in silico. Temporal, host, sequence-type (ST), and geographic patterns of resistance were modeled, with gradient-boosted machine learning algorithms predicting minimum inhibitory concentrations (MICs) based on antibiotic resistance gene profiles and chromosomal features. Temporal and geographic resistance patterns were further analyzed using statistical and visualization tools in R and Python. RESULTS:A total of 30,554 E. coli whole-genome sequences from isolates spanning 126 countries between 2000 and 2025 were analyzed. The dataset included 2015 complete genomes, 177 chromosome-level assemblies, 8310 scaffold-level assemblies, and 20,052 contig-level assemblies, with an average sequence length of 5,120,983 bp. Isolates were categorized by source: 14,320 from humans, 8184 from animals, 3941 from environmental sources, and 4109 with an unknown origin. MLST was successfully performed for 29,648 isolates, identifying dominant STs such as ST131, ST11, and ST10. Human isolates were predominantly associated with epidemic clones ST131, ST73, and ST1193, while animal isolates were frequently associated with ST10, and environmental isolates showed a strong presence of ST155. Temporal analyses indicated a steady increase in β-lactam resistance, with blaCTX-M-15, blaNDM-5, and blaOXA-1 showing the strongest increases in prevalence. Model performance was strongest for carbapenems, particularly imipenem (R2 = 0.88) and ertapenem (R2 = 0.74), whereas predictions for ampicillin and piperacillin-tazobactam showed poor agreement with observed MICs. CONCLUSIONS:This global analysis shows rising β-lactam resistance driven by key genes (blaCTX-M-15, blaNDM-5, blaOXA-1) in high-risk clones. Machine learning accurately predicted carbapenem MICs but struggled with β-lactam/β-lactamase inhibitor combinations. Integrating genomics within a One Health framework can strengthen AMR surveillance and control.
BACKGROUND:Antimicrobial resistance (AMR) in Helicobacter pylori is increasingly compromising eradication therapies worldwide. Despite growing concern, comprehensive global genomic analyses integrating resistance determinants, geographic distribution, and evolutionary patterns remain limited. METHODS:A total of 6876 high-quality H. pylori genomes collected from 85 countries between 1900 and 2024 were analyzed. Resistance determinants were identified using AMRFinderPlus, followed by lineage profiling, geographic mapping, temporal trend analysis, and resistome characterization. The distribution of virulence-associated genes and resistance gene presence patterns was also evaluated. RESULTS:Twenty-two AMR determinants were identified, predominantly chromosomal mutations. The most prevalent mutation was pbp1a S543R, associated with amoxicillin resistance, detected in 24.03% (1652/6876) of genomes across 63 countries since 1983. Fluoroquinolone resistance-associated gyrA N87K demonstrated a marked temporal increase, reaching approximately 50% prevalence by 2023. Additional gyrA and pbp1a variants were widely distributed globally. Acquired resistance genes, including blaTEM,aph(3')-IIIa, and catA1, were rare and primarily confined to sequence type 181. Among 2877 resistant isolates, 103 distinct resistance profiles were observed, with single-mutation patterns predominating. Geographic analysis revealed pbp1a S543R prevalence exceeding 40% in multiple Asian and African countries, while gyrA N87K exceeded 30% in parts of Asia and South America. The resistome exhibited an open structure, whereas 134 virulence-associated genes remained highly conserved. CONCLUSIONS:This large-scale global genomic study demonstrates the extensive dissemination and ongoing evolution of AMR in H. pylori, particularly against amoxicillin and fluoroquinolones. The findings indicate that empirical treatment strategies based on these agents are becoming increasingly unsustainable worldwide. Implementation of susceptibility-guided therapy, rapid molecular diagnostics, and international genomic surveillance programs is urgently required to preserve eradication efficacy and limit further resistance expansion.
The human gastrointestinal tract harbors trillions of microorganisms that collectively exert profound influences on host physiology, particularly immune function. Emerging evidence reveals that gut microbiota modulates immune responses through intricate interactions with host microRNAs (miRNAs), small non-coding RNAs that post-transcriptionally regulate gene expression. This review synthesizes current understanding of how gut bacteria influence host immunity via miRNA-dependent mechanisms. We examine two primary pathways: first, the capacity of gut microbes to regulate host miRNA expression profiles in immune cells and intestinal epithelium; second, the potential role of bacteria-derived small RNAs, including siRNA-like molecules, in potential cross-kingdom RNA communication (still under debate). Additionally, we explore the bidirectional nature of this interaction, whereby host miRNAs shape microbial composition and function. Comprehensive tables summarize disease-associated miRNA-microbe signatures and mechanistic pathways in immune regulation. The therapeutic implications of manipulating this axis through probiotics, dietary interventions, and miRNA-based therapies are discussed, along with future directions for translating these insights into clinical applications for inflammatory, autoimmune, and infectious diseases.
BACKGROUND:Persistent and recurrent Salmonella bacteremia remains a significant clinical challenge associated with high morbidity. The pathogen's ability to adapt within the host often leads to recurrent infections, necessitating in-depth analysis to determine if genetic heterogeneity drives this persistence. This study employs whole genome sequencing and strain phasing to investigate the evolutionary dynamics and intra-host genetic landscape of Salmonella populations in patients with persistent or recurrent bloodstream infections. METHODS:By analyzing 31 isolates from 14 patients, we used whole genome sequencing, coupled with comprehensive bioinformatics analysis, including single nucleotide polymorphisms identification, strain phasing, and phylogenetic analysis, to explore genetic heterogeneity and evolutionary patterns. RESULTS:A total of four Salmonella serotypes were identified, including S. enterica serovar Typhimurium, Typhi, Schwarzengrund, and Enteritidis, with Enteritidis being the most prevalent. Our findings revealed genetic heterogeneity shift at colony level between early and later same-patient isolates. We discovered several missense mutations in genes such as rcsB, yjiK, dsbA, glyQ and gltB, with changes in their proportions between early and later same-patient isolates. These genes are implicated in key bacterial adaptation strategies, including modulation of virulence, membrane permeability, and antibiotic resistance. CONCLUSIONS:Our research sheds light on the complex genetic landscape of Salmonella in persistent and recurrent bacteremia, highlighting the potential contribution of specific genetic mutations in the pathogen's survival and adaptability. These insights not only contribute to our understanding of Salmonella pathogenesis, but also underscore the potential for developing targeted therapeutic interventions to address the challenges posed by persistent infections.
OBJECTIVE:To investigate the polymorphism of the Rv3303c-Rv3304 intergenic region (IR) in Beijing and non-Beijing genotype Mycobacterium tuberculosis (M. tuberculosis) strains isolated from China, and to explore its regulatory effects on downstream gene expression. METHODS:A total of 223 M. tuberculosis isolates from China were classified into Beijing, non-Beijing genotype and modern Beijing subgenotype based on single nucleotide polymorphisms (SNPs). The polymorphism of Rv3303c-Rv3304 IR was identified by DNA sequencing, and a lacZ reporter system was applied to assess its regulatory role on the expression of Rv3303c. RESULTS:Of 223 isolates, 151 (67.7%) belonged to the Beijing genotype, 72 (32.3%) to the non-Beijing genotype, and 129 (85.4% of Beijing genotype strains) to the modern Beijing subgenotype. All isolates carried 1 to 7 copies of 58-bp repeating sequences in the Rv3303c-Rv3304 IR, with 3-copy repeats being the most predominant. Notably, the proportions of 3-copy repeats in Beijing and modern Beijing genotype strains were 90.1% and 90.7%, respectively, which were significantly higher than that in non-Beijing genotype strains (54.2%). β-galactosidase activity assays showed significant differences in activity among recombinant strains carrying different copy numbers of the repeating sequences (P < 0.0001). CONCLUSION:Significant differences in the polymorphism of the Rv3303c-Rv3304 IR were observed between Beijing and non-Beijing genotype M. tuberculosis strains from China. This polymorphism exhibited repeat copy-dependent regulatory activity toward the downstream gene Rv3303c in a reporter system, suggesting that it may potentially contribute to phenotypic diversity among different genotypes of M. tuberculosis.
BACKGROUND:The effective translation of scientific insights into public health action remains a challenge, despite ongoing efforts to address obesity. OBJECTIVE:To apply an infodemiological framework and examine trends in public and scientific interest from 2004 to 2023 in obesity and two behavioral and sociocultural proxy topics, the Mediterranean diet (MedDiet) and body positivity. METHODS:Data sources included Google Trends, Wikipedia page views, and SCOPUS publications. Pearson's correlation assessed linear associations. Univariate and multivariate forecasting models projected future trends. RESULTS:Scientific interest in obesity moved in parallel with MedDiet (r = 0.96) and body positivity (r = 0.89), whereas public interest measured via Google Trends were inversely associated with these topics (r = -0.62; r = -0.61). While public interest in MedDiet and body positivity aligned with scientific interest, interest in obesity per se declined over time (r = -0.89). Univariate forecasting suggests public interest in obesity will remain low through 2030, while exploratory multivariate analysis indicates a possible rebound, coinciding with a projected decline in body positivity interest. CONCLUSION:These findings reveal a divergence between scientific attention and public engagement patterns with obesity over time. While declining searches may partly reflect evolving terminology, digital trend analysis offers valuable tools for identifying gaps between research focus and public attention to support responsive, evidence-informed public health communication.
