<?xml version="1.0" encoding="utf-8"?>
    <rss version="2.0">
      <channel xmlns:content="http://purl.org/rss/1.0/modules/content/">
        <title>Frontiers in Tuberculosis | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/tuberculosis</link>
        <description>RSS Feed for Frontiers in Tuberculosis | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-10-18T02:57:00.186+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1937755</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1937755</link>
        <title><![CDATA[Translating drug-resistant tuberculosis surveillance into molecular–biophotonic diagnostic innovation in rural Eastern Cape, South Africa]]></title>
        <pubdate>2026-10-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ncomeka Sineke</author><author>Kamvelihle Sabisa</author><author>Ntandazo Dlatu</author><author>Saturnin Ombinda-Lemboumba</author><author>Teke Apalata</author><author>Lindiwe Modest Faye</author>
        <description><![CDATA[BackgroundDrug-resistant tuberculosis (DR-TB) remains a major public health challenge in South Africa, particularly in rural settings with constrained access to rapid molecular diagnostics. There is a need to identify locally relevant molecular targets that could inform the future development of affordable point-of-care (POC) diagnostic platforms. This study used routine DR-TB surveillance data to develop an epidemiology-guided framework for prioritizing molecular targets for future molecular–biophotonic diagnostic development.MethodsA retrospective secondary analysis was conducted using routine DR-TB programme data from 402 patients managed at two decentralized treatment facilities in the rural Eastern Cape Province, South Africa, between 2020 and 2024. Resistance categories, treatment outcomes, and programme vulnerability indicators were analysed descriptively. A diagnostic prioritization framework integrating disease burden, frequency of resistance categories, treatment outcome vulnerability, programme impact, and potential suitability for decentralized implementation was used to prioritize established resistance-associated molecular targets. Molecular targets were informed by published evidence; no isolate-level mutation analysis, sequencing, biosensor development, or analytical or clinical validation of a diagnostic platform was performed.ResultsRifampicin-resistant tuberculosis (RR-TB) (47.5%) and multidrug-resistant tuberculosis (MDR-TB) (44.3%) accounted for 91.8% of DR-TB cases, while pre-extensively drug-resistant tuberculosis (pre-XDR-TB) and extensively drug-resistant tuberculosis (XDR-TB) accounted for 5.7% and 2.5%, respectively. Declining treatment success and increasing proportions of unevaluated outcomes among RR-TB and MDR-TB indicated programme vulnerability; however, the available data did not permit causal attribution of these patterns to diagnostic limitations. The framework prioritized rpoB, katG, and inhA as high-priority targets, followed by gyrA, gyrB, rrs, and eis as medium-priority targets, with embB, pncA, Rv0678, atpE, and pepQ identified for future expansion. These targets were conceptually mapped to candidate biophotonic biosensing approaches; their diagnostic performance and POC suitability were not evaluated in this study.ConclusionsThis study proposes an epidemiology-guided framework for prioritizing molecular targets for future DR-TB diagnostic development in rural settings. The molecular–biophotonic component is conceptual and does not represent a validated diagnostic technology. Mutation-level characterization, biosensor development, analytical evaluation, and prospective clinical validation are required to determine the performance, feasibility, and potential POC applicability of the proposed approach.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1971442</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1971442</link>
        <title><![CDATA[Spondylodiscitis in a tuberculosis-endemic setting in Somalia: epidemiological, clinical, radiological, and outcome findings from a retrospective study]]></title>
        <pubdate>2026-10-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hussein Salad Yusuf</author><author>Abdirisak Ali Abukar</author><author>Mohamed Said Adan</author><author>Abdiaziz Siad Mohamed</author><author>Zakariye Yusuf Mohamed</author><author>Mustaf Abdi Ulusow</author><author>Mohamed Osman Dahir Alasow</author><author>Abdiwahid Ahmed Ibrahim</author><author>Naimo Awil Dahir</author>
        <description><![CDATA[BackgroundSpondylodiscitis is an important cause of spinal morbidity in tuberculosis (TB)-endemic settings, where limited microbiological capacity may complicate differentiation of tuberculous from non-tuberculous disease. Data describing the clinical spectrum and outcomes of spondylodiscitis in Somalia are limited.ObjectiveTo describe the demographic, clinical, radiological, microbiological, treatment, and outcome characteristics of patients with spondylodiscitis and to explore factors associated with clinical outcome.MethodsWe conducted a retrospective observational study of 121 eligible patients diagnosed with spinal infection at Mogadishu Somali Turkey Recep Tayyip Erdoğan Training and Research Hospital between 1 August 2023 and 31 July 2024. Demographic, clinical, radiological, microbiological, treatment, and outcome data were extracted from routine records. Associations were assessed using chi-square or Fisher's exact tests for categorical variables and Mann–Whitney U or independent-samples t-tests as appropriate for continuous variables. Outcome comparisons were restricted to patients with documented follow-up; multivariable logistic regression was not retained because only 19 unfavorable outcomes were available and outcome ascertainment was incomplete.ResultsThe mean age was 48.8 ± 18.1 years and 53.7% were male. Back pain (92.6%) and radicular pain (82.6%) were the most frequent presenting symptoms. Neurological deficit was documented in 46.3% and spinal deformity in 38.0%. Lumbar involvement was most common (48.8%), followed by thoracic involvement (25.6%); anterior-column involvement occurred in 97.5%. Epidural abscess was identified in 69.4% and is reported here as a radiological finding. Microbiological or histopathological testing was performed in 46 patients; 30 were TB-positive, corresponding to 65.2% positivity among tested patients and 24.8% confirmed TB among the total cohort. Eighty-five patients (70.2%) received empirical anti-TB treatment. Among 65 patients with documented follow-up, 46 (70.8%) achieved favorable outcomes. In bivariate analysis, TB exposure history was associated with outcome (p = 0.003), whereas operative/procedural intervention was not significantly associated with outcome (Fisher's exact p = 0.399).ConclusionSpondylodiscitis in this Somali tertiary-care cohort showed a substantial burden of neurological and radiological complications and a high proportion of empiric TB treatment. Because microbiological confirmation was limited and follow-up was incomplete, the observed confirmed TB proportion and favorable-outcome estimate should not be interpreted as population-level estimates. Prospective multicenter studies with systematic microbiological testing and complete follow-up are needed to clarify the etiological spectrum and prognostic factors.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1945832</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1945832</link>
        <title><![CDATA[Nutrition, thyroid function, and tuberculosis: exploring the endocrine–immune axis]]></title>
        <pubdate>2026-10-08T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Nooneh Khachatourian</author><author>Rubina Takhmazian</author><author>Vishwanath Venketaraman</author>
        <description><![CDATA[Tuberculosis (TB) remains a major global health challenge, with undernutrition recognized as one of the most significant modifiable risk factors influencing disease susceptibility and clinical outcomes. Emerging evidence suggests that nutritional status may also affect TB risk indirectly through its impact on thyroid function and immune regulation. This review examines the current evidence linking nutrition, thyroid dysfunction, and susceptibility to Mycobacterium tuberculosis (M. tuberculosis), with particular emphasis on the biological mechanisms that connect these factors. Essential micronutrients, including iodine, selenium, iron, zinc, and vitamin D, are critical for thyroid hormone synthesis, metabolism, antioxidant defense, and immune function. Deficiencies in these nutrients can impair thyroid physiology, disrupt endocrine homeostasis, and alter innate and adaptive immune responses that are essential for controlling M. tuberculosis infection. Thyroid hormones regulate macrophage activation, T-cell differentiation, cytokine production, immunometabolism, and oxidative stress, suggesting that thyroid dysfunction may compromise host resistance to TB. Conversely, chronic TB infection and antitubercular therapy may further disrupt thyroid function, creating a bidirectional relationship between these conditions. Collectively, the available evidence supports a conceptual framework in which nutritional deficiencies contribute to thyroid dysfunction, thyroid dysfunction impairs antimicrobial immunity, and TB further exacerbates nutritional and endocrine disturbances, establishing a self-perpetuating cycle that may increase disease susceptibility and worsen clinical outcomes. Although direct clinical evidence linking thyroid disorders with TB risk remains limited, the convergence of nutritional, endocrine, and immunological pathways provides a strong biological rationale for further investigation. Future prospective studies are needed to determine whether nutritional optimization, targeted micronutrient supplementation, and early identification and management of thyroid dysfunction can improve immune competence, reduce TB susceptibility, and enhance treatment outcomes in high-risk populations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1937953</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1937953</link>
        <title><![CDATA[High-throughput screening to identify inhibitors of the MTB CARD•RNA polymerase protein-protein interaction]]></title>
        <pubdate>2026-10-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Glory M. Velazquez</author><author>Jonathan Z. Sexton</author><author>Scott G. Franzblau</author><author>Gauri S. Shetye</author><author>Akil Hossain</author><author>George A. Garcia</author>
        <description><![CDATA[In 2023, tuberculosis (TB) once again became the world's deadliest infectious disease, overtaking COVID-19 as the leading cause of death from a single infectious agent, Mycobacterium tuberculosis (MTB). The World Health Organization (WHO) reports that the COVID-19 pandemic has reversed years of progress in providing essential TB services and reducing TB disease burden. In 2025, TB was responsible for an estimated 1.23 million deaths globally (95% uncertainty interval: 1.13–1.33 million), and there were 400 K cases of rifamycin resistant/multidrug resistant TB (RR, RIFR, MDR). While treatment success for drug susceptible TB remains high (88%), outcomes for MDR/RR-TB are lower but improving, reaching 71% globally. Clearly, there is a critical unmet need for novel antibiotics against MTB, exacerbated now due to COVID-19. The limited success in pursuing novel targets underscores the urgent need to revisit and reevaluate the mechanisms of action behind existing and once effective drugs, a strategy that may hold untapped potential in the fight against growing antibiotic-resistant TB. The MTB RNA polymerase (RNAP) is a proven target for TB treatment by rifampin (RMP), which kills both active and latent MTB. However, RMP suffers from several drawbacks including: long treatment times, activation of hPXR (inducing Cyp3A4 which is problematic for HIV-TB coinfection), and resistant mutations within RNAP. Two newer treatments with novel mechanisms of action include bedaquiline and delamanid, the former has been approved by the FDA for the treatment of multiple-drug resistant tuberculosis (MDR-MTB); however, even these new drugs already have incidences of acquired resistance. Our goal is to develop novel drug candidates for TB treatment that: target RNAP, have the potential to shorten treatment times, and have activity against RIFR mutants. Our approach, orthogonal to the rifamycins, is to target the interaction of MTB RNAP with the required transcription factor CarD. We have previously labeled CarD with the BODIPY-FL fluorophore via engineered cysteine mutations and developed a fluorescence polarization assay to monitor its interaction with RNAP and promoter DNA. Leveraging this target, we screened a 24 K small molecule library against CarD binding to MTB RNAP. We have now extended this screening to∼88,000 additional molecules.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1874315</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1874315</link>
        <title><![CDATA[Adjunctive antimycobacterial and immunomodulatory effects of Allium cepa (pink variety) in a rabbit model of latent-like mycobacterial infection]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Theophilus Kwesi Ninkyi</author><author>Eric Ogyam</author><author>Kelvin Atta Agyapong</author><author>Cynthia Amaning Danquah</author>
        <description><![CDATA[IntroductionLatent tuberculosis infection (LTBI) represents a major global reservoir for active disease, characterized by persistent, metabolically inactive bacilli that are difficult to eradicate. Novel therapeutic approaches targeting bacterial persistence and host immune responses are needed.MethodsA rabbit model of latent-like mycobacterial infection was established using aerosolized Mycobacterium aurum. The rabbits were treated with isoniazid and rifapentine (HR), ethanolic extract of Allium cepa (EAC), and combination therapy. Treatment efficacy was evaluated using colony-forming unit (CFU) counts and haematological parameters (WBC, neutrophils, lymphocytes).ResultsThe CFU counts increased significantly during the induction phase, confirming successful establishment of the latent-like mycobacterial infection model, while stabilization of bacterial load over time suggested immune-mediated containment. During the treatment phase, significant reductions in CFU counts were observed in all treated groups compared with untreated controls (p < 0.0001), with the greatest reduction seen in combination therapy groups (HR + Allium cepa extract), indicating an improved efficacy relative to monotherapy. Haematological analysis revealed significant increases in WBC, neutrophils, and lymphocytes during infection, reflecting immune activation. Treatment resulted in normalization of WBC counts, reduction in neutrophilia, and stabilization of lymphocyte levels, indicating attenuation of inflammation and restoration of immune balance.ConclusionAllium cepa demonstrated antimycobacterial and immunomodulatory effects in a rabbit model of latent-like mycobacterial infection and may have potential as an adjunctive therapeutic strategy in LTBI management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1736139</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1736139</link>
        <title><![CDATA[Secreted proteins of Mycobacterium tuberculosis as therapeutic targets for drug discovery]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Anthony Musaazi Kaweesa</author><author>Divya Tiwari</author>
        <description><![CDATA[Mycobacterium tuberculosis (M. tuberculosis), the causative agent of tuberculosis secretes proteins during the host-pathogen interaction that facilitate its survival and/or virulence within host cells. Key examples include EsxA and EsxB, CpnT/TNT, phosphatases (SapM, PtpA, PtpB), protein kinase G (PknG), the antigen 85 (ag85) complex, acyl Carrier Protein (AcpM), lipoproteins, and heat shock proteins (Hsps). Together, these secreted factors disrupt host immune responses such as phagosome maturation, antigen presentation, cytokine production, and autophagy thereby aiding in survival of these obligate intracellular bacteria. Several secreted proteins are emerging as therapeutic targets to help meet the need for shorter, more effective, and better tolerated treatment regimens for tuberculosis. Here, we review the current understanding of the major secreted proteins of M. tuberculosis. We also discuss progress in the discovery and development of drugs targeting these proteins. Overall, targeting M.tuberculosis secreted proteins remains largely in the preclinical stages of drug development. Current limitations include low potency, off-target activity, and redundancy among secreted proteins.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1814646</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1814646</link>
        <title><![CDATA[A Mycobacterium tuberculosis rare variable antigen vaccine reduces lung pathology in hypersusceptible SP140−/− mice]]></title>
        <pubdate>2026-07-15T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Zachary P. Howard</author><author>Alexander Mohapatra</author><author>Weihao Zheng</author><author>Joel D. Ernst</author>
        <description><![CDATA[Mycobacterium tuberculosis is the leading cause of death globally due to a single infectious agent. Currently, no licensed vaccine protects against pulmonary tuberculosis, the primary adult disease caused by Mtb infection. CD4 T cells are essential in protection against Mtb infection and inducing a protective CD4 T cell response remains the goal of most Mtb vaccines currently in testing. However, in contrast to other pathogens, most Mtb T cell epitopes do not exhibit sequence variation, suggesting that T cell recognition does not drive selection of escape mutants. We discovered hypothetical Mtb antigens that do exhibit sequence diversity within human T cell epitopes and tested the impact of vaccination with these rare variable antigens (RVMA) using a DNA vaccine platform. We found vaccination with RVMA significantly alters the immune response to Mtb infection in both C57BL/6 and hypersusceptible SP140‒/‒ mice without reducing lung bacterial burdens. RVMA vaccination of hypersusceptible SP140‒/‒ animals prevented necrosis and altered the lesion composition reducing tissue damage and increasing CD4 T cell distribution. Reductions in pathology were associated with increases in RORγt-expressing CD4 T cells and decreases in monocyte-derived cells in the lungs prior to the development of necrotic lesions, and were independent of B cells. These results suggest T cell responses to certain antigens may be involved in preventing pathology without significantly changing bacterial burdens and indicate that these antigens can be efficacious in Prevention of Disease TB vaccines.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1855903</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1855903</link>
        <title><![CDATA[Implementation of sequencing-based surveillance for drug-resistant tuberculosis in Nigeria]]></title>
        <pubdate>2026-07-02T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Heather P. McLaughlin</author><author>Israel Audu</author><author>Monday Tola</author><author>Chika Kingsley Onwuamah</author><author>Julius Ogwu</author><author>Kenneth Atoe</author><author>Chioma Nneka Kunle-Ope</author><author>Isiyaku Ahmadu</author><author>Joshua Gowon</author><author>David B. Meshak</author><author>Mosunmola Iwakun</author><author>Chinedu Ejianya Ude</author><author>Modupe Abiona</author><author>Abidemi Esther Momoh</author><author>Temiloluwa Ore</author><author>Chinenye Angela Ogbu</author><author>Temitope Abigail Abiodun</author><author>Jamie Dawson</author><author>Patricia Hall-Eidson</author><author>Nnaemeka C. Iriemenam</author><author>McPaul Okoye</author><author>Clement Adesigbin</author><author>Obioma Chijioke-Akaniro</author><author>Elom Emeka</author><author>Anyaike Chukwuma</author>
        <description><![CDATA[Sequencing for drug-resistant tuberculosis (DR-TB) surveillance was established in Nigeria for the first time, demonstrating a nationally coordinated referral network for multi-disease sequencing services. Mycobacterium tuberculosis isolates previously identified as resistant to rifampicin and/or isoniazid by genotypic or phenotypic drug susceptibility testing were selected proportionately across all six geopolitical zones in Nigeria. Programmatic use of sequence data for DR-TB surveillance was prioritized, demonstrating additional resistance detection and enhanced monitoring as new TB treatment regimens are scaled up. Sanger sequencing identified resistance to rifampicin and isoniazid missed by drug susceptibility tests routinely used in country, for 11% (5/47) and 2% (1/47) of isolates, respectively. This pilot study demonstrates feasibility and provides an example for programmatic implementation of integrated sequencing, supporting country efforts to strengthen genomic surveillance for DR-TB and improve prevention and control globally.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1830528</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1830528</link>
        <title><![CDATA[The AcasR-FadD9 regulatory axis modulates iron homeostasis and susceptibility to the anti-mycobacterial compound ACA]]></title>
        <pubdate>2026-06-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Feng Huang</author><author>Zixin Wang</author><author>Dong Jiang</author><author>Shengyi Li</author><author>Zheng-Guo He</author><author>Hua Zhang</author>
        <description><![CDATA[Mycobacterial drug resistance leads to prolonged treatment, increased mortality, and increased healthcare costs. In this study, 3-azidothiophene-2-carboxylic acid (ACA), a dual-targeting inhibitor of the cell assembly proteins CpsA1 and CpsA2, exerted its activity through an iron-dependent pathway. The screening of drug-resistant mutants revealed that a frameshift mutation in the transcriptional regulator acasR (BCG_0932/Rv0880) conferred ACA resistance. Conversely, acasR overexpression increased bacterial susceptibility. Furthermore, AcasR specifically bound to and repressed the promoter of fadD9 (Rv2590), which was its sole functionally validated target under the tested conditions. Crucially, fadD9 overexpression phenocopied ACA resistance, whereas its deletion heightened susceptibility. Integrated omics and iron assays revealed that ACA induced intracellular iron starvation, a condition exacerbated by fadD9 deletion. These findings reveal a novel resistance pathway in which AcasR modulates mycobacterial drug susceptibility by repressing fadD9, which in turn affects siderophore-mediated iron homeostasis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1853414</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1853414</link>
        <title><![CDATA[Using interpretable decision trees to explore TB-HIV integration under data constraints: a proof-of-concept analysis]]></title>
        <pubdate>2026-06-25T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ntandazo Dlatu</author><author>Lindiwe Modest Faye</author><author>Mojisola Clara Hosu</author><author>Teke Apalata</author>
        <description><![CDATA[BackgroundStrengthening tuberculosis (TB) and HIV service integration remains a major priority in resource-limited settings, where fragmented care contributes to delayed diagnosis, poor treatment continuity, and suboptimal patient outcomes. Evaluating implementation conditions associated with integrated care remains challenging because health system data are often simplified, inconsistently recorded, and insufficiently structured to capture the complexity of real-world service-delivery processes. This study aimed to demonstrate the application of an interpretable decision-tree framework to explore selected implementation and service-delivery conditions associated with TB-HIV integration using a highly constrained secondary dataset.MethodsA quantitative exploratory proof-of-concept analysis was conducted using a simplified secondary dataset comprising 10 TB-HIV integration implementation cases. Funding, healthcare worker training, patient education, medication access, and infection control were included as binary implementation indicators and entered simultaneously into the decision-tree model. The Gini index was used descriptively to assess node impurity and decision structure. Correlation network analysis was performed to examine patterns of variable alignment, with Pearson correlation coefficients (equivalent to the phi coefficient for binary variables) interpreted solely as descriptive indicators of co-occurrence within the dataset. Given the extremely small sample size and simplified binary structure, all analyses were exploratory and illustrative rather than predictive, inferential, or causal.ResultsFunding emerged as the primary discriminating variable in the decision tree, with all cases reporting increased funding classified as successful (6/6) and all cases without increased funding classified as unsuccessful (4/4). Although all implementation variables were evaluated by the algorithm, no additional variable provided sufficient information gain to generate further branching. Descriptive correlation analysis indicated alignment between funding and TB-HIV integration outcomes (r = 0.78), healthcare worker training (r = 0.76), patient education (r = 0.62), and infection control (r = 0.58). These coefficients are presented solely as descriptive indicators of variable alignment and should not be interpreted as measures of effect size, association strength, or statistical evidence.ConclusionThis proof-of-concept study demonstrates how interpretable decision-tree approaches can be used to explore implementation conditions associated with TB-HIV integration under severe data constraints. The findings do not identify determinants of integration success but rather illustrate how selected implementation conditions were structured within a constrained analytical framework. The study highlights both the utility and limitations of interpretable analytical approaches when applied to small, dichotomized health systems datasets. Future research should employ larger, more granular, process-sensitive, and contextually rich datasets to support robust evaluation of TB-HIV integration in real-world settings.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1854329</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1854329</link>
        <title><![CDATA[Identification of novel DNA gyrase B inhibitors in Mycobacterium species using integrated computational approaches]]></title>
        <pubdate>2026-06-18T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jagritee Yadav</author><author> Lalhmangaihzuali</author><author>Harish Shukla</author><author>Anshuman Chandra</author><author>Sudhir Kumar Singh</author><author>Meenakshi Singh</author>
        <description><![CDATA[IntroductionDrug-resistant Mycobacterium tuberculosis remains a major global health challenge, particularly due to the emergence of multidrug-resistant and extensively drug-resistant strains. DNA gyrase, specifically the ATPase domain of GyrB, represents a promising target for the development of novel anti-tubercular agents.MethodsA comprehensive computational workflow was employed, including pharmacophore-based virtual screening of approximately 1,000,000 compounds from the PubChem, ZINC, ChEMBL, and MolPort databases. Hits were filtered using Lipinski's rule of five, structural diversity analysis, molecular docking, ADMET and toxicity assessment, molecular dynamics simulations, and density functional theory analyses.ResultsApproximately 30,000 preliminary hits were obtained, which were reduced to 21 candidate molecules and subsequently to 10 unique compounds. Molecular docking identified two lead compounds, D (PubChem ID: 166484985) and I (PubChem ID: 166484904), with strong binding affinity toward the GyrB ATPase domain. ADMET and toxicity analyses indicated favorable drug-likeness and safety profiles. Molecular dynamics simulations and density functional theory studies further confirmed stable protein-ligand interactions and significant electronic reactivity.DiscussionCompounds D and I demonstrated promising ATP-competitive inhibition of the GyrB ATPase domain and exhibited distinct species-specific interaction profiles. These findings support their potential as novel anti-tubercular lead scaffolds for further experimental validation and therapeutic development.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1855780</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1855780</link>
        <title><![CDATA[Genomic characterization of drug-resistant Mycobacterium tuberculosis complex in western Kenya reveals predominance of isoniazid resistance and discordance with routine susceptibility testing]]></title>
        <pubdate>2026-06-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Susan Musau</author><author>Susan Odera</author><author>Victor Moses Musyoki</author><author>Eleanor I. Lamont</author><author>Noel Onyango</author><author>Bob Morrison</author><author>Wilfred Murithi</author><author>Steve Wandiga</author><author>Videlis Nduba</author><author>David Sherman</author><author>Marianne W. Mureithi</author>
        <description><![CDATA[IntroductionWhole-genome sequencing (WGS) data on resistance patterns in western Kenya remain limited. We evaluated resistant patterns of Mycobacterium tuberculosis complex (MTBC) isolates from western Kenya based on routine line probe assay (LPA) and/or phenotypic drug-susceptibility testing (DST) using targeted WGS.MethodsIn this cross-sectional study, 1,053 archived MTBC isolates from 12 counties in western Kenya were analyzed. An enriched subset of 316 isolates was selected for WGS, of which 290 produced high-quality genomes. Genomic data were analyzed to determine lineage distribution and identify drug resistance mutations using WHO mutation catalogue.ResultsOut of the 1,053 isolates, 127 (12%) showed resistance to at least one anti-TB drug. Isoniazid resistant-rifampicin susceptible (Hr-TB) isolates were the most common (52; 40%), followed by rifampicin-resistant (33;26%) and multidrug-resistant (23;18%). The predominance of Hr-TB is consistent with reports from Kenya and other high-burden settings. Enriched WGS subset identified resistance-associated mutations in 43/290 (14%) isolates, with similar resistance patterns. Rifampicin resistance was mainly associated with rpoB (S450L), while isoniazid resistance was dominated by katG S315 T and inhA promoter mutations. Resistant isolates were mainly concentrated in Kisii, Migori, Homa Bay, and Siaya, predominantly within Lineages 4 and 3. Discordance was observed between routine testing and WGS (p = 0.026); approximately 86% of discordant isolates carrying mutations of uncertain significance.ConclusionWestern Kenya shows geographic DR-TB heterogeneity with predominant Hr-TB, which rifampicin-based diagnostics risk under-detection. Despite observed discordance, Integrating WGS with routine testing will strengthen surveillance, improve isoniazid resistance detection, and support appropriate treatment management in high-burden settings.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1781507</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1781507</link>
        <title><![CDATA[Differential roles of resident lung macrophages during control of murine alveolar and airway Mycobacterium abscessus infection]]></title>
        <pubdate>2026-06-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kelsey C. Haist</author><author>Jack H. Congel</author><author>Jodi M. Corley</author><author>Alma E. Ochoa</author><author>Jazalle McClendon</author><author>Patrick S. Hume</author><author>Jerry A. Nick</author><author>William J. Janssen</author><author>Kenneth C. Malcolm</author><author>Katherine B. Hisert</author>
        <description><![CDATA[IntroductionMycobacterium abscessus (Mabsc), a nontuberculous mycobacterium (NTM), is readily cleared from healthy lungs but can cause infections in immunocompromised individuals and individuals with chronic airways diseases that disrupt mucociliary clearance, such as cystic fibrosis and bronchiectasis. In bronchiectatic airways, Mabsc can persist despite robust immune cell recruitment, raising the possibility that, in addition to impaired mucociliary clearance, local pulmonary immune defects contribute to NTM susceptibility. Since chronic infections result from failed eradication of acute infection, we sought to determine whether immune cell responses critical for control of acute Mabsc infection in healthy lungs remain relevant when Mabsc infection occurs in obstructed airways, rather than in the alveoli, as occurs in bronchiectasis.MethodsUsing an agar bead model of Mabsc infection that prolongs murine small airway infection, replicates factors associated with bronchiectasis, and mirrors pathology of human Mabsc lung disease, we tested the hypothesis that Mabsc infection in obstructed airways elicits a qualitatively different immune response that alveolar Mabsc infection. We compared myeloid cell responses in in the two infection models using flow cytometric analyses of lung cells, immunofluorescent imaging, and histopathologic evaluation of lung sections.ResultsDuring the first 2 weeks of the bead model of Mabsc infection, absolute abundance of neutrophils in the lungs was significantly higher and relative abundance of recruited macrophages was lower than in the alveolar Mabsc infection model. Additionally, most resident alveolar macrophages (CD11c+ RAMs) in the bead model upregulated CD11b, a marker of inflammation, by 1-week post-infection and maintained high levels of CD11b expression at 3 weeks post infection despite infection occurring in airways, not alveoli. To understand the role of macrophage subsets in controlling Mabsc infection, clodronate liposomes were administered oropharyngeally to deplete RAMs. RAMs were essential for early control of alveolar Mabsc infection, but depletion of RAMs had no effect on control of Mabsc burden during bead infection.ConclusionsThese studies demonstrate that murine Mabsc airway infection induced by obstructing small airways with Mabsc embedded in agar beads generates an immune milieu distinct from that induced by Mabsc infection in alveoli, altering the importance of different macrophage populations for control of infection.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1797268</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1797268</link>
        <title><![CDATA[Sigma factor M induces an ESX-4-focused regulon in Mycobacterium abscessus]]></title>
        <pubdate>2026-06-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jill G. Canestrari</author><author>Shawn Gianola</author><author>Keith M. Derbyshire</author><author>Todd A. Gray</author>
        <description><![CDATA[Mycobacteria encode as many as five distinct Type VII (ESX) secretion systems that function in nutrient acquisition, cell-cell interaction, membrane integrity and pathogenesis. The biological activities of ESX systems are determined by the effector proteins they secrete. ESX-4 is the ancestral secretion system and is conserved throughout mycobacteria, including Mycobacterium abscessus where it has been shown to support survival in phagosomes. ESX-4 and putative effector genes in Mycobacterium tuberculosis and Mycobacterium smegmatis are co-induced by a conserved sigma factor, SigM. Identifying the activities conferred by ESX-4 in promoting M. abscessus survival begins with identifying potential secreted substrates. We hypothesized that, in M. abscessus, SigM co-regulates the expression of genes encoding ESX-4 components and secreted effector proteins. We generated a precise deletion of the sigM-rsmA locus, encoding SigM and its dedicated anti-sigma factor. Performing RNA-seq using this deletion strain and a SigM-expressing complementation derivative, we identified SigM-responsive mRNAs in M. abscessus. Analysis of responsive promoters defined a consensus SigM-binding site, indicating direct induction by SigM. Together these data defined 15 SigM-targeted loci transcribing 50 genes with annotations and structures consistent with ESX secretion. While SigM induces multiple esx4 locus promoters in M. smegmatis, only the promoter encoding the primary EsxU/EsxT secreted substrates are direct targets in M. abscessus, suggesting that production of the secretion apparatus is controlled by other transcription factors. The putative effector complexes identified here present strong candidates for the pathogenic roles previously reported for ESX-4 in M. abscessus infection models.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1740382</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1740382</link>
        <title><![CDATA[Non-tuberculous mycobacteria pulmonary disease in Texas: an analysis of 8 years of hospital discharge data]]></title>
        <pubdate>2026-05-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Alex Baham</author><author>Jotam G. Pasipanodya</author><author>Devanshi Mehta</author><author>Susan McBride</author><author>Shashikant Srivastava</author>
        <description><![CDATA[BackgroundNon-tuberculous mycobacterial (NTM) pulmonary disease (PD) is a recognized chronic condition associated with high healthcare utilization. Texas statewide NTM diagnosis-coded inpatient discharges per 100,000 discharge records (healthcare utilization) have not been systematically studied.MethodsWe analyzed Texas hospital inpatient discharge public use data between 2016 and 2023 for all 254 Texas counties. MS-EXCEL and SPSS were used for data collection and analysis.ResultsOut of 23.33 million hospital discharge records, 12,587 were identified to have an NTM diagnosis-coded inpatient discharge. Among the patients with NTM, 3.3% of the patients were aged 0–17 years, 19.5% were 18–44 years, 29.5% were 45–64 years, and 47.7% were 65 + years old. The NTM diagnosis-coded inpatient discharge rate in Texas was calculated to be 59.9/100,000 records (range 46.1–62.6). A total of 815 NTM cases were reported in Northeast Texas and 4,203 cases in the Gulf Coast counties. The total number of in-hospital deaths among the NTM-coded discharges was 692 (5.5% of total NTM cases). The number of patients with NTM covered under Medicare Part A was 5,102 and 1,521 were on Medicaid.ConclusionsBased on the hospital discharge data analysis, there appears to be regional variation in the prevalence of NTM disease in Texas. Further studies are needed to determine these variations and to improve our understanding of NTM-PD in Texas.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1805962</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1805962</link>
        <title><![CDATA[Research overview—2025: integrating scientific progress to accelerate global tuberculosis elimination]]></title>
        <pubdate>2026-05-26T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Patrick K. Moonan</author><author>Timothy H. Holtz</author>
        <description><![CDATA[Major scientific advances across the tuberculosis research continuum emerged in 2025, offering new opportunities to accelerate progress toward global elimination. This review synthesizes developments in diagnosis, treatment, prevention, and post-disease care, highlighting innovations that broaden access, strengthen mechanistic insight, and expand the scope of actionable tools. Diagnostic progress included artificial intelligence–enabled chest imaging, noninvasive molecular testing using tongue and stool samples, simple stool-based procedures suitable for decentralized settings, biomarkers that support treatment monitoring, low-complexity nucleic acid tests for extrapulmonary disease, and new point-of-care methods for detecting infection. Culture-free sequencing approaches further improved rapid identification of drug resistance. Therapeutic advances featured shorter all-oral regimens for drug-susceptible and rifampin-resistant disease, along with emerging compounds that target essential microbial pathways. Additional progress in host-directed therapies, vaccines, and nanoparticle-based drug delivery broadened preventive and therapeutic options. Conceptual developments challenged the validity of symptom-based disease categories and supported biologically grounded terminology, while consensus definitions for post-tuberculosis lung disease clarified the substantial long-term respiratory burden among survivors. Despite this momentum, health-system limitations and inequitable access continue to constrain real-world impact. Collectively, the scientific advances of 2025 were substantial and outline a clearer mechanistic and programmatic path toward tuberculosis elimination, but their success will depend on effective implementation and integration into routine care.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1809118</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1809118</link>
        <title><![CDATA[Readiness assessment as a strategy, not an afterthought: leveraging implementation science to integrate tuberculosis comorbidity care in Pakistan's health system]]></title>
        <pubdate>2026-04-23T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Saima Aleem</author><author>Zohaib Khan</author><author>Bilal Ahmad Khan</author><author> Zala</author><author>Saima Afaq</author>
        <description><![CDATA[Health facility readiness assessment is a foundational element in designing and implementing integrated tuberculosis (TB) and comorbidity interventions, particularly in low- and middle-income countries (LMICs) like Pakistan. The integration of TB care with management of comorbid conditions like diabetes mellitus, depression, and tobacco use is complicated and challenged by diverse, multifaceted barriers at the health system, organizational, and individual levels. Evidence-based frameworks, such as Consolidated Framework for Implementation Research (CFIR), Reach, Effectiveness, Adoption, Implementation, and Maintenance (RE-AIM) framework, the Exploration, Preparation, Implementation, Sustainment (EPIS) framework, and related tools, help researchers to systematically evaluate service system capacity for service delivery, determine operational gaps and shortcomings, and understand socio-cultural and infrastructural constraints. This ensures that subsequent interventions are not only scientifically grounded but also tailored and well-suited to local capacities, thereby enhancing the sustainability and overall effectiveness of integration. In this perspective paper, we argue that readiness assessment should be institutionalized that is, formally embedded within service delivery structure, routine policy, planning, and decision-making processes, as a strategic prerequisite for integrating tuberculosis and comorbidity care, and we highlight how implementation science frameworks can support context-sensitive planning and scale-up in Pakistan and other similar health system settings.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1750007</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1750007</link>
        <title><![CDATA[Evaluation of the performance of promising host transcriptional biosignatures in predicting TB progression during a 1-year prospective cohort study in Indian household contacts]]></title>
        <pubdate>2026-04-17T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Synne Jenum</author><author>Steffen Hadasch</author><author>Dhanasekaran Sivakumaran</author><author>Christina Skår Saghaug</author><author>Jonas Høgberg</author><author>Kasama Chusang Larsen</author><author>Sumithra Selvan</author><author>Helene Larsen</author><author>Christian Ritz</author><author>Harleen M. S. Grewal</author>
        <description><![CDATA[IntroductionAchieving the goal of the End TB Strategy depends on new tools, preferably blood-based point-of-care (POC) tests, to identify individuals at risk of progression from M. tuberculosis infection to subclinical or clinical tuberculosis (TB). A decade of signature discovery and validation has resulted in several transcriptional signatures with promising capacity for predicting TB progression within the next 3–6 months, but evaluation of signature performance in Asian populations is lacking.MethodsNested within a prospective observational cohort study of Indian household contacts (HHC study), we adapted the RISK6 and Sweeney3 along with our locally derived INDIA11 signature to the microfluidic RT-qPCR platform (Fluidigm) and evaluated their capacity to predict TB progression during a 12-month follow-up in a head-to-head comparison. As readily available in our dataset, the recently published single-gene signatures GBP2, FCGR1B, and SERPING1 were also assessed.ResultsOf the 525 recruited household contacts, 12 (6 cases in children aged 5–14 years) progressed to TB (5 at 6 months, 7 at 12 months) as defined by growth of M. tuberculosis in respiratory specimens. RISK6 and Sweeney3 were successfully adapted to the Fluidigm platform. One gene in the INDIA11 assay failed, resulting in the INDIA10 signature with an overall failure rate of 5.7%. RISK6, Sweeney3, and INDIA10 demonstrated comparable but statistically non-significant predictive performance for TB progression, with AUCs: RISK6 0.61 (95%CI 0.41–0.82), Sweeney3 0.61 (95%CI 0.41–0.80), INDIA10 0.59 (95%CI 0.46–0.72). Applying a fixed value of sensitivity 75% corresponding to the WHO minimum target for TB prediction resulted in the corresponding specificities RISK6 0.49 (95%CI 0.41–0.56), Sweeney3 0.32 (95%CI 0.25–0.39), and INDIA10 0.42 (95%CI 0.35–0.50). Of single-gene signatures, the AUCs of FCGR1B and GBP2 were significant with specificities of FCGR1B 0.56 (95%CL 0.49–0.64) and GBP 0.50 (95%CL 0.43–0.58).DiscussionThe expression of interferon-gamma–inducible gene signatures were able to discriminate between TB progressors and non-progressors in an hitherto underexplored Indian population, supporting the generalizability of RNA technology to this setting. Given the limited sensitivity and specificity of current biosignatures in all populations, exploration of integrated diagnostic algorithms relying on established and novel tools in a multidisciplinary approach is warranted.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1783887</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1783887</link>
        <title><![CDATA[Immunometabolic reprogramming of Mycobacterium tuberculosis-responsive memory CD4+ T cell subsets is linked to long-term protective immunity]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Vaishnavi Kaipilyawar</author><author>Samantha Leong</author><author>Arianne Lovey</author><author>Lorenzzo L. Stringari</author><author>Reynaldo Dietze</author><author>Jerrold J. Ellner</author><author>Rodrigo Ribeiro-Rodrigues</author><author>Padmini Salgame</author>
        <description><![CDATA[IntroductionMemory CD4+ T cells are central to long-term immunity in tuberculosis (TB), yet their functional roles that define their protective capacity remain unclear. Understanding the immune mechanisms that prevent clinical progression from latent TB infection (LTBI) to active TB disease is critical for the development of next-generation vaccines and biomarkers.MethodsWe characterized the transcriptomic, metabolic, and functional programs of Mycobacterium tuberculosis (Mtb) antigen-stimulated peripheral CD4+ T stem cell (T-SCM), central (T-CM), transitional (T-TM), and effector (T-EM) memory subsets from individuals with remote LTBI. We utilized a multi-platform validation strategy that integrated RNA-sequencing data with protein-level metabolic profiling using “Met-Flow” cytometry and functional growth restriction assays to link memory CD4+ T cell differentiation states to immunometabolism and antimycobacterial function. Finally, we evaluated the immunometabolic profiles of memory CD4+ T cell subsets in an independent, longitudinal cohort of Mtb-exposed progressors and non-progressors from Brazil (GSE112104).ResultsWe identified a differentiation gradient associated with distinct immunometabolic states. T-SCM and T-CM subsets exhibited elevated mitochondrial activity and oxidative metabolism (fatty acid oxidation), supporting their proliferative capacity. In contrast, T-TM and T-EM subsets underwent glycolytic reprogramming and engaged the pentose phosphate pathway, which fueled enhanced cytokine production and Mtb growth restriction. Importantly, we observed that non-progressors exhibit fatty acid oxidation-driven, stem/central memory-like signatures, while progressors and active TB cases display elevated exhaustion markers, glycolytic reprogramming and pro-inflammatory profiles aligned with disease progression.ConclusionCollectively, findings from our proof-of-concept study suggest metabolic state as a key axis connecting Mtb antigen-induced memory T cell differentiation, restimulation-induced transcriptional programming, and durability of immune control. The findings provide the basis for future longitudinal studies to examine the dynamic metabolic and functional modulation in Mtb antigen-specific memory T cell subsets from contained infection to disease progression.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/ftubr.2026.1819209</guid>
        <link>https://www.frontiersin.org/articles/10.3389/ftubr.2026.1819209</link>
        <title><![CDATA[Editorial: Non-tuberculous mycobacteria and bronchiectasis]]></title>
        <pubdate>2026-04-01T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Octavio M. Rivero-Lezcano</author><author>Ramiro López-Medrano</author><author>Jaime Esteban</author>
        <description></description>
      </item>
      </channel>
    </rss>