Background Ebola virus disease (EVD) remains a serious public health hazard due to high mortality, multiple modes of transmission, and persistence in the environment. The existing Ebola transmission models have been constrained to a single or two-population framework, which are insufficient to capture multiple-population interaction transmission structures. Methods This study proposes a multi-population autonomous Ebola transmission model with Susceptible, Exposed, Infectious, Hospitalized, Recovered, and Deceased infected corpse compartments and a shared viral reservoir in the environment. This model proposes that transmission is direct, hospital-acquired, corpse-mediated, and indirect environmental, and these modes are documented by a bilinear incidence formulation. Results Positivity and boundedness properties of solutions were established via a mathematical analysis, and the basic reproduction number was derived using the next-generation matrix approach. The analytical findings show that whereas supercritical transmission results in persistent behaviour and the occurrence of endemic equilibria under the suggested parameters, the disease-free equilibrium is stable under the subcritical transmission condition. Conclusions The numerical simulations support the applicability of the suggested multi-population paradigm for comprehending threshold-dependent Ebola transmission behaviour and show its qualitative dynamics under various transmission conditions.
Nipah virus, a highly lethal zoonotic paramyxovirus with a case‑fatality rate of 40-75%, poses a formidable threat to global health security. This review synthesizes its evolving epidemiology, contrasting the Malaysian and Bangladesh‑India strains, and dissects molecular pathogenesis focusing on G/F glycoprotein recognition of ephrin receptors and the multi‑layered immune evasion mediated by P gene products. Phylogenetic analyses reveal 8-10% nucleotide divergence between lineages, with positive selection in the G protein that may compromise vaccine cross‑protection. Ecological risk amplifiers-deforestation and climate‑driven habitat loss-reshape spillover dynamics through spatial expansion of bat foraging, prolonged risk windows, and pathway diversification. Deforestation exceeding 5% per decade correlates with a 2-3‑fold increase in spillover events in Bangladesh. A dynamic risk‑assessment framework is proposed that views pandemic potential as the convergence of viral evolution, ecological amplification, and geographic expansion-from South Asia to Pteropus‑bearing regions worldwide, including unrecognized risks in China. Current medical countermeasures (mRNA vaccines, m102.4 antibody, remdesivir) and deployment challenges (genetic diversity, biosafety level 4 constraints, regulatory dependence on the "Animal Rule") are evaluated. The conclusion calls for a "One Health"‑informed global defense system anchored on four pillars: intelligent forecasting that integrates ecological data; a broadly protective countermeasure repository; democratized rapid diagnostics; and translational bridges linking molecular insights to actionable interventions. Strengthening global collaboration is imperative to prevent Nipah virus from escalating into a pandemic.
Background Rotaviruses are major pathogens of childhood acute gastroenteritis, dominated by rotavirus A (RVA). Outbreaks caused by human rotavirus C (RVC) are rarely reported, and relevant genomic data remain scarce. This genomic investigation of an RVC outbreak improves our understanding of viral diversity and transmission dynamics. Methods We performed epidemiological surveys, nucleic acid testing and whole-genome sequencing (WGS) on specimens from a 2025 RVC-associated gastroenteritis outbreak at a Chinese boarding high school. Sequence alignment, phylogenetic and molecular tracing analyses were conducted to explore RVC evolution via point mutation, segment reassortment and genomic recombination. Results This typical point-source campus outbreak was linked to an indoor student gathering matching the incubation period of RVC. Thirteen RVC FX strains were recovered from 11 rectal swabs and two vomitus samples. Their viral protein (VP) 4 and VP7 sequences shared high homology with Russian reference strains, carrying distinct amino acid variations. No segment reassortment or recombination was detected in VP4/VP7 genes. Conclusions Dense, closed campus settings facilitate RVC clustered transmission. Limitations included absent screening of asymptomatic canteen staff. Rapid nucleic acid testing enabled timely pathogen identification for outbreak control. Greater attention should be paid to the public health risk of RVC. These whole-genome sequencing data enrich resources for studying RVC evolution and vaccine development.
Background Severe fever with thrombocytopenia syndrome (SFTS) caused by severe fever with thrombocytopenia syndrome virus (SFTSV) has become a persistent threat to public health. Since neutralizing monoclonal antibody therapy can invoke an immediate and effective passive immunity, endeavours made to discover the therapeutic monoclonal antibodies should be worthwhile. This study aimed to screen and purify the human monoclonal antibodies (hmAbs) against SFTSV glycoprotein C and characterize the properties of the hmAbs. Methods Human monoclonal antibodies (hmAbs) against SFTSV glycoprotein C (Gc) were prepared from the convalescent SFTS patients’ lymphocytes using the phage display technology. A single-chain variable fragment antibody library against SFTSV Gc was successfully constructed, and two specific single-chain variable fragment antibodies were screened and expressed as hmAbs immunoglobulin G (IgG) (hIgG4 and hIgG5). Results Enzyme-linked immunosorbent assay, Western blot and immunofluorescence assay test results confirmed that both hIgG4 and hIgG5 specifically bound to SFTSV Gc antigen and intact SFTSV virions. The neutralization test showed that both hmAbs exhibited broad-spectrum neutralizing activity against three SFTSV strains with different genotypes (A, E and F) in vitro. By analyzing the RNA level of M segment by reverse transcription-polymerase chain reaction, the SFTSVs’ RNA levels were decreased, specifically, the RNA of SFTS virus JS3, SFTS virus JS4 and Phlebovirus JS2010-014 was reduced by 79%, 80% and 87% respectively for hIgG4, and the value was 88%, 87% and 89% for hIgG5. According to the observation of the cytopathic effect, the minimal protective concentration of hIgG4 and hIgG5 was 62.5 μg/mL and 31.25 μg/mL respectively. Conclusions hIgG4 and hIgG5 possess potent neutralizing effects, showing great potential as candidate therapeutic hmAbs for SFTS treatment.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection progresses from an initial direct viral cell injury to an immune-mediated response. In most cases, the immune response results in viral clearance and recovery after a mild disease. Severe infections seem to result mainly from uncontrolled immune-mediated damage. Accordingly, initial treatment involves an antiviral strategy, while late severe infection is treated with anti-inflammatory medication. Immunocompromised patients have reduced vaccine efficacy and reduced ability to mount an appropriate immune response to SARS-CoV-2 infection, making them extremely susceptible to prolonged and severe infections. For these patients, standard treatment protocols need further investigation. In this retrospective case series, we investigated the effect of convalescent plasma and late antiviral treatment in twenty-three immunosuppressed patients, mostly pre-vaccinated (91%), presenting with symptomatic prolonged SARS-CoV-2 infection. All patients received initial antiviral treatment at the time of the first confirmed SARS-CoV-2 infection but continued to have symptoms. Convalescent plasma in addition to other treatments, including antivirals, resulted in significant improvement in 22 patients. Statistically significant improvement was detected in oxygen supplementation requirement (69.5% vs. 48%, p = 0.025), fever (61% ± 0.96 vs. 4% ± 0.42, p = 0.001), and C-reactive protein (9.6 ± 7.64 vs. 5.05 ± 5.05, p = 0.007). Interestingly, increases in white blood cell counts were found to be good predictors of improvement in this population. Our data suggest that CCP and antiviral treatment in the later phases of coronavirus disease 2019 may be necessary for immunosuppressed individuals with prolonged disease.
Background Pyrimidine metabolism is crucial for the replication of viruses and the functionality of host cells. However, the cell-type-specific organization of this metabolism in the central nervous system and its dysregulation during Japanese encephalitis virus (JEV) infection remain poorly understood. Here, we aimed to characterize the cell-type-specific landscape of pyrimidine metabolism in the CNS and uncover pyrimidine metabolic reprogramming during JEV infection. Methods Single-cell RNA sequencing data from normal and JEV-infected mouse brains were analyzed to profile the expression of pyrimidine metabolic genes across neuronal, glial, and vascular cell types. Functional validation of these metabolic pathways on JEV replication was performed in Neuro-2a cells and primary mouse brain-derived mixed neuron/glia cultures using pharmacological inhibitors, metabolite supplementation, and virological assays, including quantitative reverse transcription polymerase chain reaction, immunoblotting, and plaque assay. Results We defined a universal core program for pyrimidine homeostasis alongside specialized, function-oriented metabolic programs across neurons, glia, and vascular cells in the normal mouse brain. JEV infection triggered cell-intrinsic reprogramming of this metabolic network, with viral replication critically depending on the de novo pyrimidine biosynthesis pathway in neurons. Pharmacological inhibition of the key enzyme dihydroorotate dehydrogenase significantly suppressed JEV replication. Furthermore, JEV replication created a metabolic dependency on exogenous glutamine and enhanced glutamate oxaloacetate transaminase-mediated aspartate synthesis for precursor acquisition. Conclusions JEV rewires host brain pyrimidine metabolism in a cell-type-specific manner, revealing distinct metabolic dependencies on de novo pyrimidine biosynthesis, exogenous glutamine uptake, and glutamate oxaloacetate transaminase-mediated aspartate synthesis in neurons and highlighting potential targets for future antiviral strategies. By resolving these alterations at single-cell resolution, this study also provides a cell-type-resolved pyrimidine metabolic landscape of both the normal and JEV-infected brain.
Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to evolve and mutate during transmission, making the development of effective broad-spectrum antibodies for the prevention and treatment of SARS-CoV-2 infections of great significance. In this study, peripheral blood mononuclear cells (PBMCs) were isolated from 15 convalescent coronavirus disease 2019 (COVID-19) patients to construct a human-derived single-chain variable fragment (scFv) antibody library against SARS-CoV-2. Monoclonal antibodies targeting the conserved structural region of the spike glycoprotein subunit 2 (S2) protein with broad-spectrum neutralizing activity were subsequently screened. Methods The cDNA of the PBMCs from 15 convalescent COVID-19 patients was used to amplify the human-derived antibody heavy chain variable region (VH) and light chain variable region (VL) via polymerase chain reaction (PCR). The VH and VL genes were randomly assembled into scFvs using overlap extension PCR. The constructed scFv gene library was cloned into the phage display vector pComb3XSS and electroporated into XL1-Blue cells to generate a human SARS-CoV-2 scFv antibody library. Then monoclonal antibodies specific to the SARS-CoV-2 S2 domain were screened by phage display. Gene sequencing and recombinant human immunoglobulin G (IgG) monoclonal antibody expression were performed to produce human IgG antibody. The antibody was subsequently evaluated for its binding ability and neutralizing activity against different viral subtypes. Furthermore, the fragment antigen-binding region of the selected antibody was modeled using structure prediction tools to support subsequent structural analysis. Results The library size of the constructed human-derived SARS-CoV-2 single-chain antibody library (scFv library) is 1.6 × 10⁷ CFU. The S2-specific full-length IgG antibody (IgG-S2) was selected and expressed, which demonstrated neutralizing activity against both the SARS-CoV-2 wild type strain and the Omicron variant. Conclusions A human single-chain antibody library against SARS-CoV-2 was successfully constructed. From this library, a human antibody targeting the highly conserved S2 region of SARS-CoV-2 was selected, which exhibited broad-spectrum neutralizing activity. This antibody shows potent in vitro neutralizing activity and offers a preliminary molecular basis for the subsequent development of SARS-CoV-2 therapeutics and broad-spectrum vaccines.
Oropouche virus (OROV) is an emerging orthobunyavirus that causes increasingly severe and deadly disease in Brazil. However, coinfection with influenza A(H1N1)pdm09 has not been previously described in the published literature, to our knowledge. We report the first documented fatal case of OROV and influenza A(H1N1)pdm09 coinfection in a previously healthy 16-year-old female from rural Maranhão, Brazil. The patient presented with dyspnea, odynophagia, and hemoptysis and deteriorated rapidly, requiring orotracheal intubation on day three of illness due to massive endobronchial hemorrhage, followed by fatal hemodynamic collapse. Autopsy revealed bilateral serosanguineous pleural effusion, diffuse alveolar hemorrhage, pericardial petechiae, acute tubular necrosis, and cerebral edema with tonsillar herniation. Real-time reverse-transcriptase polymerase chain reaction confirmed OROV in lung, liver, spleen, and lymph node tissues, and influenza A(H1N1)pdm09 in both nasal swab and lung tissue; all other arboviruses and respiratory pathogens tested negative. The histopathological findings provide, to our knowledge, the first histopathological characterization of OROV-associated microvascular injury and suggest synergistic thromboinflammatory pathways with influenza A.This case broadens the recognized clinical spectrum of OROV and highlights the need for systematic coinfection screening and coagulation monitoring in severe arboviral presentations, even in young patients without comorbidities.
Bundibugyo ebolavirus (BDBV), a member of the genus Orthoebolavirus, family Filoviridae, is hereafter referred to as Bundibugyo virus, with the associated illness termed Bundibugyo virus disease (BVD). First identified in Uganda in 2007, the virus has received far less scientific attention than the highly pathogenic Zaire ebolavirus. In April 2026, a cluster of unexplained deaths emerged in the mining-intensive Mongbwalu Health Zone of Ituri Province in the Democratic Republic of the Congo (DRC), and the causative agent was confirmed by whole-genome sequencing on 14 May 2026 as Bundibugyo virus. This is the DRC's 17th Ebola outbreak and only the third BVD epidemic globally. As of 10 June 2026, the DRC has reported 662 confirmed cases and 124 confirmed deaths, with the outbreak expanding across 25 health zones in Ituri, North Kivu, and South Kivu provinces; Uganda has reported 19 confirmed cases and 2 deaths. Unlike Zaire ebolavirus outbreaks, no licensed vaccine or specific therapeutic exists for BVD, and the response is further complicated by armed conflict, population mobility through mining corridors, fragile health systems, and community mistrust that has occasionally erupted into violence against responders. The World Health Organization (WHO) declared a Public Health Emergency of International Concern (PHEIC) on 17 May 2026, and the Africa Centres for Disease Control and Prevention (Africa CDC) declared a Public Health Emergency of Continental Security (PHECS) on 18 May 2026. Under a unified "One Team, One Plan, One Budget, and One M&E Framework" architecture, the Africa Centres for Disease Control and Prevention and World Health Organization jointly issued the Bundibugyo Virus Disease Continental Preparedness and Response Plan, with a budget of $517.7 million over six months and structured around 14 technical pillars. This review provides a comprehensive synthesis of the virology, epidemiology, critical research gaps, and international response strategy, aiming to inform both ongoing outbreak operations and future scientific efforts.
The coronavirus disease 2019 (COVID-19) pandemic has exposed profound and persistent weaknesses in global preparedness, including fragmented surveillance systems, governance failures, inequitable access to countermeasures, and erosion of public trust. Although SARS-CoV-2 has dominated global attention, other high-consequence zoonotic pathogens with pandemic potential have remained comparatively neglected. Among these, the Nipah virus (NiV) represents a particularly serious threat, characterized by high case-fatality rates, zoonotic spillover from wildlife reservoirs, documented human-to-human transmission, and the absence of licensed vaccines or specific antiviral therapies. This narrative review synthesizes and contextualizes existing evidence on the NiV through the lens of lessons learned during the COVID-19 pandemic. Drawing on epidemiological data, outbreak experience, and global health policy literature, this review examines the key dimensions of preparedness, including surveillance and diagnostics, laboratory and health-system capacity, vaccine and therapeutic development, emergency governance, ethical decision-making, and the operationalization of One Health approaches, with particular attention to low- and middle-income and fragile settings. The review highlights that despite scientific advances achieved during COVID-19, preparedness for the NiV remains limited and uneven. Persistent gaps in integrated surveillance at human-animal-environment interfaces, constrained laboratory capacity, insufficient investment in countermeasures, fragmented governance, and enduring global inequities threaten timely detection and containment. The NiV should therefore be understood not as an isolated regional concern, but as a warning signal for future "Disease X" scenarios, underscoring the urgent need to translate COVID-19 lessons into sustained, equitable, and multisectoral pandemic preparedness.
Background:Shigella spp. remains a major cause of diarrheal disease globally, with escalating antimicrobial resistance and high transmissibility posing persistent public health threats. However, large-scale spatiotemporal genomic analyses are scarce, particularly for the neglected species S. boydii and S. dysenteriae, limiting global surveillance and vaccine development. Methods:We curated 42,189 Shigella genomes from worldwide sources (1914-2024) and performed systematic genomic characterization on 17,360 high-quality genomes using in silico serotyping, core-genome multilocus sequence typing (cgMLST), and antimicrobial resistance gene (ARG) analysis. Results:This largest dataset to date encompasses 68 countries across six continents, yet sampling is heavily skewed toward high-income regions. We identified 50 serotypes and 166 sequence types (STs), uncovering strong serotype-ST associations and pronounced geographical predilections. Critically, the distribution of predominant serotypes reveals gaps in coverage by current vaccine candidates in some high-burden settings. cgMLST provided molecular evidence for extensive cross-border transmission, particularly among S. flexneri and S. sonnei. ARGs were detected in 99.74% of genomes, with carriage rates displaying distinct continental patterns and significant temporal increases for quinolone, macrolide, and extended-spectrum β-lactamase genes; the colistin resistance gene mcr-1.1 was identified in S. sonnei. Notably, the under-characterized species S. boydii and S. dysenteriae exhibited considerable serotype diversity and international dissemination. Conclusions:This study delivers the most comprehensive spatiotemporal and species-inclusive genomic resource for Shigella to date, unveiling serotype gaps in vaccine strategies, cross-border transmission dynamics, and spatiotemporal variations in resistance gene distribution.
Background:While the acute phase of the COVID-19 pandemic has passed, understanding its pathophysiology remains critical for managing long-term sequelae and future viral threats. Oxidative stress is a proposed key driver of COVID-19 severity, but its relationship with the dynamic inflammatory cascade and its value as a standalone biomarker requires further validation. Methods:Case-control study was conducted to quantify systemic oxidative stress burden in 109 hospitalized COVID-19 patients (56 severe, 53 mild-moderate) and 112 healthy controls. Serum total oxidant status (TOS) and total antioxidant status (TAS) were measured, and the oxidative stress index (OSI) was calculated and correlated to the inflammatory mediators (IL-6, IL-8, IL-10, IP-10, CRP, SAA). Results:COVID-19 patients exhibited a profound redox imbalance, characterized by elevated TOS and OSI, and depleted TAS compared to controls (p < 0.05). This imbalance was exacerbated in severe disease, where TOS and OSI were significantly increased. The OSI demonstrated superior diagnostic performance for disease severity (AUC = 0.90; 95% CI: 0.86-0.95) compared to TOS (AUC = 0.89) and TAS (AUC = 0.78). Crucially, both TOS and OSI showed strong positive correlations with inflammatory cytokines and acute-phase proteins (IL-6, IL-10, IP-10, CRP, SAA; all p < 0.001). After adjusting for age, time from symptom onset, and comorbidity burden (Charlson Comorbidity Index), multivariate analysis confirmed that high OSI was independently associated with disease severity (adjusted OR: 4.8; 95% CI: 1.9-12.1). Conclusions:The OSI is a robust, integrative biomarker that strongly reflects COVID-19 severity and is closely linked to the hyperinflammatory state. The OSI is strongly correlated with increased inflammatory cytokines and acute-phase proteins in acute COVID-19.
Background:Antimicrobial resistance is a growing global public health concern, posing a serious threat to human health. This study aimed to characterize the composition and distribution of microbial communities, metal resistance genes (MRGs), antibiotic resistance genes (ARGs), and virulence factor genes (VFGs) under multi-metal stress and assess the impacts of metal and soil properties on the diversity, abundance, carrying rate (proportion of gene carriers), co-occurrence rate (proportion of microorganisms co-carrying multiple gene types), and mobility potential (MP, likelihood of horizontal gene transfer) of these genes. Methods:Soil samples were collected from eight sampling sites within a metal mining area (metal-contaminated soil group, MS) and four sites located more than 3 km away from the mining area (control group). Metal concentrations and physicochemical properties of the soils were measured using standard methods. Metagenomic sequencing was performed to characterize the composition and distribution of the microbiome, resistome, and virulome. Statistical modeling was applied to examine the effects of heavy metal content and soil properties on the relative abundance, co-occurrence, and mobilome potential of the three gene types. Results:Fe, V, Cr, and Cu primarily promoted the diversity, carrying rate, and co-occurrence rate of microbial communities, MRGs, ARGs, and VFGs. In contrast, Ni and Zn exhibited overall inhibitory effects. For every unit increase in Fe and V, the MP of MRGs and VFGs was associated with an increase of 3.0 × 10⁻⁵ and 1.2 × 10⁻⁵, respectively. A per 1 mg/kg increase in Cr and Cu was correlated with a decrease of 4.3 × 10⁻⁵ and 1.1 × 10⁻⁴ in the MP of ARGs and of MRGs, respectively. Positive correlations were found between the MP of plasmid‑mediated ARGs and Cr, and between transposon‑mediated ARGs and Cr/V. The MP of transposon‑mediated MRGs correlated positively with Fe, while Cu correlated negatively with plasmid‑mediated ARGs but positively with insertion sequence‑mediated ARGs. Ni concentration was positively associated with the MP of IS‑mediated VFGs. Conclusions:Metals alter the composition and distribution of microbial communities, MRGs, ARGs, and VFGs. A key mechanism underlying this regulation is the modulation of their mobile potential, which either facilitates or restricts horizontal gene transfer.
Background:The implementation of the National Centralized Drug Procurement (NCDP) policy has had far-reaching effects. This study aims to assess the impact of the NCDP policy on the disease burden of lower respiratory infections (LRIs) in China. Methods:The age-standardized incidence rates (ASIR), age-standardized mortality rates (ASMR), and age-standardized disability-adjusted life-years rates (ASDR) from the Global Burden of Disease (GBD) 2021 database were used to describe the disease burden and compare it before (1990-2017) and after (2019-2021) the implementation of the NCDP policy. We applied interrupted time series (ITS) analysis to assess changes in the burden of LRIs before and after policy implementation, with 2018 designated as the intervention cutoff year. Results:The ITS analysis revealed a consistent declining trend in the ASIR, ASMR, and ASDR for LRIs in China from 1990 to 2021. Following the implementation of the NCDP policy in 2018, all three indicators showed a statistically significant acceleration in reduction. The ASIR decreased from 5,481.13 to 2,853.81 per 100,000 population. Following policy implementation (2019-2021), the slope of the ASIR was estimated to be -185.73, also indicating a statistically significant declining trend (β₃ = -109.45, p = 0.001). Similarly, the ASMR declined from 60.65 to 14.03 per 100,000, with the slope changing from -1.69 (p < 0.001) to -3.18 (p = 0.006). The ASDR also demonstrated a significant reduction from 3,128.39 to 347.67 per 100,000, with the trend slope accelerating from -101.66 (p < 0.001) to -196.36 (p = 0.007) after policy implementation. All models were adjusted for first-order autocorrelation using the Prais-Winsten method. Conclusions:After the implementation of the NCDP policy, the disease burden of LRIs in China decreased, suggesting that the policy effectively reduced the disease burden on patients.
Cerebral malaria (CM) remains one of the most severe and life-threatening manifestations of Plasmodium falciparum infection, predominantly affecting children and pregnant women in Sub-Saharan Africa, where resource constraints compound diagnostic and therapeutic challenges. Despite significant advances in antimalarial therapy, CM continues to be associated with high mortality rates (15%–30%) and significant long-term neurological sequelae among survivors (10%–30%). Challenges in the diagnosis and management of CM in resource-limited African settings, include widespread misdiagnosis (up to 23% of clinically diagnosed CM cases may not meet strict diagnostic criteria), delayed presentation, inadequate supportive care infrastructure, and limited access to specialized neurological rehabilitation services. The lack of fundoscopic examination, neuroimaging capabilities, and reliable biomarkers in most African healthcare facilities compounds diagnostic challenges. Treatment delays due to poor referral systems, geographical barriers, and inadequate transportation significantly impact patient outcomes. In this review, the practical challenges of diagnosing and managing CM in resource-limited African healthcare settings, an area inadequately addressed in existing literature, is discussed while providing context-appropriate recommendations for each identified barrier. We address health systems constraints including workforce shortages, supply chain disruptions, and absent rehabilitation services for CM survivors. By synthesizing current evidence and highlighting critical gaps, this review aims to inform policy makers, clinicians, and researchers about priority areas for intervention to reduce CM-associated morbidity and mortality in African regions.
The advent of advanced molecular technologies, particularly the widespread use of next-generation sequencing (NGS), has revolutionized the life sciences research landscape. NGS, characterized by high throughput, specificity, and sensitivity, offers a superior alternative to traditional detection methods, particularly in the context of viral pandemics and emerging infectious diseases. It has proven indispensable not only in identifying novel therapeutic targets but also in monitoring viral resistance. This review provides a comprehensive analysis of NGS applications in infectious diseases and pathogenic microorganisms, with an emphasis on its role in rapid pathogen detection, accurate identification, interspecies transmission tracking, and resistance profiling. Through the integration of these insights, the review offers a forward-looking perspective on emerging trends and challenges, highlighting the transformative impact of these technologies on the understanding and management of infectious diseases.
Background:Tuberculosis (TB) remains a major global cause of mortality and is a leading cause of death among women of reproductive age (WRA). Untreated TB in this population endangers both maternal and neonatal health, yet the age-stratified burden and the shifting distribution of drug-resistant tuberculosis remain poorly defined in global health agendas. This study aims to employ data from the 2021 Global Burden of Disease Study to systematically evaluate the global, regional, and age-specific burden of TB among WRA, to delineate temporal trends in drug-resistant TB, and to assess associated risk factors using standardized estimation methods. Methods:Leveraging data from the Global Burden of Disease Study 2021 covering 204 countries and territories, we systematically assessed TB burden in WRA aged 15-49 years from 1990 to 2021. We analyzed age-standardized incidence, prevalence, mortality, and disability-adjusted life years across socio-demographic index (SDI) regions, TB subtypes, and risk factors. Projections to 2030 were generated using autoregressive integrated moving average models. Results:Between 1990 and 2021, the global prevalence and incidence of TB among WRA declined significantly. However, this decline was uneven across age groups, disease types, and regions. TB incidence peaked in women aged 15-24 years, while mortality and disease burden were highest among those aged 45-49 years. Drug-resistant tuberculosis was most prominent in the 25-29 age group. Geographically, sub-Saharan Africa remained the core of the global TB burden, with BRICS (Brazil, Russia, India, China, South Africa) countries carrying significantly higher burdens than G7 countries. Risk attribution patterns revealed a shift from behavioral to metabolic drivers, with high body mass index emerging as the leading risk factor in high-SDI regions. Middle-SDI regions showed a combination of metabolic and behavioral risks, while metabolic factors remained dominant in low-SDI settings. Drug-susceptible tuberculosis was primarily linked to smoking and malnutrition, whereas drug-resistant tuberculosis was increasingly associated with metabolic dysfunction. Conclusions:Despite global declines in TB prevalence and incidence among WRA, stark disparities persist. The age-stratified rise in drug-resistant TB, particularly in resource-constrained regions, underscores the need for targeted, gender-responsive interventions that integrate infectious disease control with metabolic health strategies.
