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Journal articleBarnes M, Stretch S, Swieboda D, et al., 2026,
Mucosal IL-36 is a defining feature of severe paediatric bronchiolitis
, Mucosal Immunology, ISSN: 1933-0219RationaleBronchiolitis is the commonest cause of hospital admission in children under the age of 1 year, most cases being due to respiratory syncytial virus (RSV) infection. The mechanisms causing infantile bronchiolitis are incompletely understood but include a deficient mucosal interferon response, neutrophilic inflammation and enhanced mucosal Type-2 responses.ObjectivesWe sought to determine the mucosal immune processes associated with severe paediatric bronchiolitis.MethodsWe performed transcriptomic analyses on mucosal samples from infants hospitalized with Moderate (n = 48) and Severe (n = 40) bronchiolitis. Differential expression and regression analyses determined genes associated with different severity categories. Responses were modelled in vitro using air–liquid interface human nasal epithelial cell culture models.Measurements and main resultsWe confirmed weakened interferon-associated signalling in severe RSV and non-RSV bronchiolitis but unexpectedly found elevated IL-36α (an IL-1 family cytokine implicated in chronic inflammatory diseases) early in infection. Conversely, IL36A was decreased in whole blood during severe RSV, suggesting that this association is unique to the mucosa. In human nasal epithelial cells grown in vitro under air–liquid interface we found IL-36α to be produced by epithelial cells during RSV infection and that its secretion is enhanced by neutrophils.ConclusionsThese findings implicate mucosal IL-36α as a dominant feature of severe paediatric bronchiolitis.
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Journal articleTomas Catala A, 2026,
In vivo functional profiling and structural characterisation of the human GLP1R A316T variant
, Science Advances, ISSN: 2375-2548Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are effective therapies for type 2 diabetes (T2D)and obesity, yet patient responses are variable, with GLP1R gene variation potentially linked to therapeutic outcomes. A GLP1R natural missense variant, A316T, protects against T2D and cardiovascular disease. Here, we generated and characterised a human GLP1R A316T mouse model. Human GLP1RA316T/A316T mice displayed lower fasting blood glucose versus wildtype littermates even under metabolic stress, as well as slower weight gain and alterations in islet cytoarchitecture, glucagon secretion and liver metabolism under a high-fat, high sucrose diet. This was however associated with blunted responses to pharmacological GLP-1RAs in vivo. Further investigations in b-cell models demonstrated that human GLP1R A316T exhibits characteristics of constitutive activation but dampened GLP-1RA responses. Results are further supported by cryo-EM analyses and molecular dynamics simulations of GLP-1R A316T structure, collectively demonstrating that the A316T variant governs basal GLP-1R activity and pharmacological responses to GLP-1R-targeting therapies.
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Journal articleSanchez-Garcia MA, Sadiku P, Ortmann BM, et al., 2026,
Author correction: Hypoxia induces histone clipping and H3K4me3 loss in neutrophil progenitors resulting in long-term impairment of neutrophil immunity
, Nature Immunology, Vol: 27, ISSN: 1529-2908Correction to: Nature Immunology https://doi.org/10.1038/s41590-025-02301-9, published online 28 October 2025.In the version of this article initially published, the surname of Musa M. Mhlanga was misspelled (Mhalanga) and is now amended in the HTML and PDF versions of the article.
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Journal articleMqadi L, Bedwell GJ, Msolo N, et al., 2026,
Distress is positively associated with induced secondary hyperalgesia in people with suppressed HIV☆
, JOURNAL OF PAIN, Vol: 39, ISSN: 1526-5900 -
Journal articleKnox-Brown B, Robertson L, Amaral A, et al., 2026,
Physiological quotients and mortality: redefining lung function interpretation beyond FEV1
, European Respiratory Journal, ISSN: 0903-1936 -
Journal articleWagstaffe HR, Thwaites RS, Sidhu JK, et al., 2026,
Pre-existing and early cellular immune factors correlate with functionally complete protection against primary controlled human SARS-CoV-2 infection
, Nature Communications, Vol: 17, ISSN: 2041-1723Identifying host factors that mediate protection during first exposure to newly emergent viruses may assist in responding to future pandemics. Here, we report correlates of protection in a controlled human infection model of SARS-CoV-2 in serologically naïve individuals (n=34, aged 18-29 years) inoculated with 10 TCID50 of a D614G-containing pre-Alpha variant SARS-CoV-2. Eighteen developed “sustained infection” and seroconverted, while the remaining 16 did not. Pre-exposure and early immune factors associated with resisting infection were comprehensively analysed using multiplex protein, cytometric and RNA sequencing approaches in the upper respiratory mucosa and circulation. Associations between pre-existing antibody level and outcome suggested a modest role for cross-reactive antibodies in protection, with baseline nasal anti-SARS-CoV-2 Spike IgM levels correlating with delayed infection onset. Instead, resistance to infection was associated with heightened nasopharyngeal CCL13 levels produced locally by conventional dendritic cells and monocytes. Cross-reactive IL-2 producing T cells against SARS-CoV-2 non-structural proteins and less differentiated NK cells were also enriched at the time of inoculation in these individuals. This was followed by increased numbers of innate and adaptive cellsin the nasopharynx, including resident memory T cells, within 24 hours of virus exposure. Conditional independence network analysis revealed nasal CCL13 as the central node in a module associated with protection, connected to pre-existing RTC-specific T cells by CD1c+ DCs. In those who became infected, higher baseline cross-reactive T cell and less differentiated NK cell frequencies also correlated with shorter duration of infection. Thus, enhanced pre-existing mucosal chemokine levels may enable rapid immune cell recruitment and antigen-presentation to resident T cells in respiratory mucosa, effectively blocking infection. Where this local response fails to c
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Journal articleKobiela A, Klimczuk M, Serafin PK, et al., 2026,
Remodeling of the cell membrane-associated protein pool affects adhesive membrane properties in filaggrin insufficient keratinocytes and impacts distinct cellular and organellar functions
, BMC Biology, Vol: 24, ISSN: 1741-7007BackgroundAtopic dermatitis (AD) is a highly prevalent inflammatory skin disease, affecting up to 30% of children at some point in their life and frequently persisting into adulthood. Insufficiency in the late epidermal protein filaggrin is frequently observed in the lesional skin of patients, with direct and indirect impact on the skin barrier quality and function. We hypothesized that filaggrin reduction influences intracellular, surface, and derived extracellular membranes of keratinocytes with multiple impacts on the cell function.ResultsUsing filaggrin knockdown keratinocytes generated by shRNA interference (shFLG), we determined that the physical characteristics of the cellular membranes (reported by refractive index) are changed on a filaggrin insufficiency background. Using proteomics, protein binding modeling, and functional assays, we established that filaggrin insufficiency in keratinocytes results in changes in both organelles comprised of internal cellular membranes (i.e., small extracellular vesicles, sEVs) and the plasma membrane. We detected increased association of anti-adhesive proteins (tenascin-C and matrilin-2) with sEVs, resulting in a reduction of the fibronectin-1-mediated sEV uptake by dendritic cell subsets. At the same time, dysregulation of the tight junction and cell adhesion molecules at the level of the cell increased keratinocyte adhesiveness to reconstituted basement membrane substratum as well as faster gap closure in the wound healing assay. We also independently confirmed the findings on sEV uptake and wound healing in filaggrin knockout N/TERT-2G keratinocytes, which more closely resemble primary cells.ConclusionsWe conclude that the alterations in different membrane compartments in filaggrin insufficiency are reflected in changes in keratinocyte functions of relevance to AD pathology, and strategies to target those could open up new therapeutic approaches.
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Journal articleMcKenzie J, Carter C, Jackson MM, et al., 2026,
Mechanisms driving immunopathogenesis of viral exacerbations in chronic respiratory disease.
, ThoraxBACKGROUND: Exacerbations are major causes of morbidity in individuals with chronic respiratory diseases such as chronic obstructive pulmonary disease, asthma and bronchiectasis. Increasing evidence implicates respiratory viruses as predominant triggers, though the underlying immunopathogenic mechanisms remain poorly understood. NARRATIVE: This review synthesises current knowledge on the interplay between viral pathogens at the airway epithelial barrier, including structural and immunological mechanisms that may dysregulate antiviral immunity in chronic respiratory diseases. Furthermore, we discuss how perturbations in the respiratory microbiome, characterised by reduced microbial diversity, can modulate host antiviral immune defences. CONCLUSIONS: Collectively, these interconnected factors create a permissive environment predisposing to viral infection and exacerbations in chronic respiratory diseases. Understanding the complex interactions between airway structure, interferon-mediated antiviral responses, inflammation and microbiota is essential for developing targeted therapies to effectively manage virus-induced exacerbations and reduce disease burden.
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Journal articleMartyn O, Vlasich C, Khariv V, et al., 2026,
Global epidemiology and disease burden of human parainfluenza virus in adults: a systematic review
, Reviews in Medical Virology, Vol: 36, ISSN: 1052-9276Parainfluenza virus (PIV) is a common cause of respiratory illness in children and immunocompromised adults, but little is known about its epidemiology or disease burden in the general adult population. This review evaluates published global epidemiological and disease burden for PIV in adults, including high-risk patients (immunocompromised or with chronic illnesses), and identifies existing data gaps. A PRISMA systematic review of publications from 2014 to 2023 in PubMed reporting PIV prevalence and disease burden (including hospitalisations, mortality) in adults (≥ 18 years) and high-risk patients was performed. Sixty-five studies were included; which skewed towards Asia, Europe, and North America, highlighting a data gap in global PIV prevalence. Overall prevalence of PIV (all strains) ranged from 0 to 15.2% [median 2%] in the general adult population (not considered high-risk but tested for infection). PIV3 was the most prevalent strain (0.6−15.2% [2.9]), followed by PIV4 (0.4−6.5% [1.9]), PIV1 (0.5−2.8% [1.1]), and PIV2 (0−2.9% [1.1]). PIV prevalence was generally higher in high-risk adults (up to 41% in certain risk groups) and those aged ≥ 65. Mortality rates ranged from 2 to 40% in those high-risk, while need for respiratory assistance ranged from 0.9% to 64.2% and hospitalisation from 3.7% to 45.3%. None of the studies reported cost-related healthcare resource utilisation. Variability of study designs, data stratification, and patient populations in the selected studies challenged evaluating the true prevalence of PIV and its burden. PIV infection carries an underappreciated burden, with substantial morbidity and mortality risks, especially in high-risk patients. Significant knowledge gaps exist regarding global prevalence and economic burden in the general adult population.
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Journal articleMah JSY, Eng PC, Izzi-Engbeaya C, et al., 2026,
The role of glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter-2 inhibitors in chronic obstructive pulmonary disease.
, Expert Rev Clin Immunol, Vol: 22, Pages: 31-41INTRODUCTION: Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of morbidity and mortality worldwide, with type 2 diabetes mellitus (T2DM), obesity, and cardiovascular disease being common co-morbidities associated with worse outcomes. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter-2 (SGLT2) inhibitors, which were originally developed for treatment of T2DM and/or obesity, have recently been shown to reduce exacerbations in observational studies of patients with COPD, suggesting that repurposing GLP-1RAs and SGLT2 inhibitors could improve clinical outcomes in COPD. AREAS COVERED: COPD, diabetes, and obesity share several common inflammatory pathways, including macrophage dysfunction, inflammasome activation, and metabolic dysregulation. Here we review the pharmacology, pre-clinical, and emerging clinical data which could support repurposing of GLP-1RAs and SGLT2 inhibitors for use in COPD through a search of articles in PubMed and Medline from 01/1950 to 08/2025. EXPERT OPINION: Reevaluating metabolic therapeutic targets has the potential to redefine treatment strategies for patients with COPD and metabolic comorbidities. Potential mechanisms of action could be via modulation of the NLRP3 inflammasome and macrophage polarization or better control of co-morbid conditions. However, randomized controlled trials and mechanistic studies are needed to confirm these observational findings and elucidate underlying mechanisms.
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Journal articleFeleszko W, Caminati M, Gern JE, et al., 2026,
Effect of tezepelumab on asthma exacerbations co-occurring with infection-attributed acute respiratory illnesses.
, Ann Allergy Asthma Immunol, Vol: 136, Pages: 61-65.e1BACKGROUND: Tezepelumab, a human monoclonal antibody, blocks the activity of thymic stromal lymphopoietin. In the phase 2b PATHWAY (NCT02054130) and phase 3 NAVIGATOR (NCT03347279) studies, tezepelumab reduced exacerbations and improved lung function, asthma control, and health-related quality of life vs placebo in patients with severe, uncontrolled asthma. OBJECTIVE: To evaluate the incidence of asthma exacerbations co-occurring with documented acute respiratory illnesses attributed to infections. METHODS: Patients were randomized 1:1 to receive tezepelumab 210 mg subcutaneously or placebo every 4 weeks for 52 weeks. The incidence of asthma exacerbations co-occurring with respiratory illness-related adverse events (AEs) was assessed. Co-occurrence was defined as at least 1 day of overlap between a respiratory illness-related AE and the asthma exacerbation period beginning 7 days before the start of the exacerbation until the end of the asthma exacerbation. RESULTS: Of the 1334 patients (tezepelumab, n = 665; placebo, n = 669) included, 312 experienced at least 1 asthma exacerbation co-occurring with a respiratory illness-related AE attributed to an infection. The incidence of asthma exacerbation co-occurring with a respiratory illness-related AE was lower in the tezepelumab group than in the placebo group overall (18.2% vs 28.6%; exposure-adjusted incidence difference [EAID], -11.1 [95% CI: -15.75, -6.41]) and among patients with perennial allergy (EAID, -11.6 [95% CI: -17.44, -5.69]) and without perennial allergy (EAID, -10.2 [95% CI: -18.16, -2.10]). CONCLUSION: Tezepelumab reduced asthma exacerbations attributed to respiratory infections in patients with severe, uncontrolled asthma compared with placebo, irrespective of perennial allergy status. TRIAL REGISTRATION: This is a pooled analysis of 2 studies registered at Clinicaltrials.gov: PATHWAY (NCT02054130) and NAVIGATOR (NCT03347279).
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Journal articleCorren J, Reid F, Moate R, et al., 2026,
FRONTIER-3: a randomised phase 2a study to investigate tozorakimab, an anti-interleukin-33 monoclonal antibody, in early-onset asthma.
, ERJ Open Res, Vol: 12, ISSN: 2312-0541BACKGROUND: Interleukin (IL)-33 is implicated in the initiation and progression of asthma. FRONTIER-3 (NCT04570657) was a phase 2a study to investigate tozorakimab, an anti-IL-33 monoclonal antibody, in adults with moderate-to-severe early-onset asthma receiving standard of care. METHODS: Patients were randomised 1:1:1 to tozorakimab 600 mg, tozorakimab 300 mg or placebo, once every 4 weeks subcutaneously. The primary end-point was change from baseline to week 16 in pre-bronchodilator (pre-BD) forced expiratory volume in 1 s (FEV1) measured in clinic. Secondary and exploratory end-points included home pre-BD FEV1, home peak expiratory flow (PEF), rescue medication use, CompEx, pharmacokinetics, immunogenicity and safety. RESULTS: The intent-to-treat (ITT) population included 235 patients with a median disease duration of >30 years; a majority had a baseline blood eosinophil count (BEC) <300 cells·μL-1. At week 16, tozorakimab did not show a statistically significant improvement in change from baseline in clinic pre-BD FEV1 versus placebo (least-squares mean difference (LSMD) (80% CI), 600 mg: 4 mL (-71-79), p=0.473; 300 mg: 36 mL (-38-111), p=0.267). Compared with the ITT population, a pre-specified subgroup of patients with ≥2 prior exacerbations showed greater improvements in clinic pre-BD FEV1 at week 16 with tozorakimab versus placebo (LSMD (80% CI), 600 mg: 212 mL (102-322), p=0.007; 300 mg: 77 mL (-34-187), p=0.186). Tozorakimab also showed greater improvements in home FEV1 and home PEF versus placebo at week 16 in patients with ≥2 prior exacerbations than in the ITT population. Tozorakimab was well tolerated. CONCLUSIONS: Although FRONTIER-3 did not meet the primary study end-point, tozorakimab treatment showed encouraging efficacy signals in patients with early-onset asthma and a history of exacerbations.
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Journal articleTangara B, Barsosio HC, Marlais T, et al., 2026,
Artemether-lumefantrine versus pyronaridine-artesunate for the treatment of malaria in patients with mild to moderate COVID-19 in Kenya and Burkina Faso: a randomised open-label trial (MALCOV).
, EClinicalMedicine, Vol: 91BACKGROUND: It is unknown whether the choice of malaria treatment for uncomplicated malaria affects coronavirus disease 2019 (COVID-19) severity, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral load, or duration of viral shedding. Several antimalarials exhibit antiviral activity against SARS-CoV-2 in vitro and have been suggested as potential therapeutic candidates for COVID-19, particularly pyronaridine-artesunate (PA), despite disappointing clinical results with chloroquine and hydroxychloroquine. METHODS: We conducted an open-label randomised trial comparing standard 3-day treatment with PA and artemether-lumefantrine (AL) in newly diagnosed SARS-CoV-2 infected patients aged ≥6 months with rapid diagnostic test or microscopy-confirmed non-severe malaria in Kenya and Burkina Faso. SARS-CoV-2 was assessed by RT-PCR on days 3, 7, 14, and 28, and symptom resolution was assessed daily for 14 days using FLU-PRO Plus. The primary endpoint was the proportion of participants with SARS-CoV-2 clearance by day 7. Secondary endpoints included SARS-CoV-2 clearance by days 14, 21, and 28, time to SARS-CoV-2 clearance over 28 days, median viral load on day 7, and time to symptom resolution. Complete case analysis was conducted using log-binomial regression for binary outcomes, Cox-regression for time-to-event outcomes, and negative binomial regression for count outcomes, all adjusted for disease severity and viral load at enrolment. The trial is registered with ClinicalTrials.gov NCT04695197. FINDINGS: From January 2021 to January 2022, 143 participants were randomised (PA = 69, AL = 74, intention-to-treat [ITT] population), including 117 with reverse transcription polymerase chain reaction (RT-PCR) confirmed (PA = 58, AL = 59, modified intention-to-treat [mITT] population) and 26 with rapid-antigen test confirmed SARS-CoV-2 infection. The median age was 19 years (interquartile range [IQR] 13-38), 66% were aged ≥15 years. Baseline characteristics were co
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Journal articleJia X, Foo IJ, McQuilten HA, et al., 2026,
Influenza virus infection drives upregulation of CD84 across a broad range of immune cells.
, Clin Transl Immunology, Vol: 15, ISSN: 2050-0068OBJECTIVES: Our previous study in hospitalised patients infected with avian A(H7N9) influenza virus identified CD84 amongst several genes associated with recovery. Yet, the correlation between CD84 and respiratory viral infection outcomes is far from established. We aimed to define CD84 dynamics in patient cohorts of respiratory disease and immune cell populations in influenza virus-infected mice. METHODS: Expression dynamics of CD84 and association with previously identified correlates of severe and fatal respiratory disease outcomes, OLAH and IL18R1, were analysed in A(H7N9) and COVID-19 patient cohorts across disease severities. Using mouse models of influenza virus infection, CD84 expression on immune cell subsets was analysed over the course of infection. RESULTS: Elevated CD84 levels in recovered A(H7N9) patients were accompanied by increased expression of genes for CD84-associated adaptor proteins and other SLAM receptor family members. In these patients, high CD84 expression persisted until discharge, while remaining low throughout the disease in patients that succumbed. We found inverse correlations between CD84 with OLAH and IL18R1 levels in our A(H7N9) cohort, and in hospitalised COVID-19 patients across respiratory disease severities. In influenza virus-infected mice, CD84 was upregulated on a broad range of immune cell populations, particularly on activated and influenza virus-specific T-cell populations and correlated with less disease severity. CONCLUSION: Our findings revealed the link between high CD84 expression in humans and recovery from respiratory viral infections. In mice, CD84 expression increased across a broad range of immune cell populations, with CD84 expression on activated T-cell populations correlating with less severe disease.
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Journal articleNamporn T, Manopwisedjaroen S, Ngodngamthaweesuk M, et al., 2025,
Evidence of Mpox clade IIb infection in primary human alveolar epithelium
, EMERGING MICROBES & INFECTIONS, Vol: 14 -
Journal articlePolineni D, Davies JC, Boyd AC, et al., 2025,
Potential gene therapies for cystic fibrosis: a plain language summary for non-specialists and the lay community
, Future Rare Diseases, Vol: 5 -
Journal articleAhmed R, Mulupi S, Taegtmeyer M, et al., 2025,
“People here live in denial”: A qualitative study of the pervasive impact of stigma on asthma diagnosis and care in Kenya and Sudan
, Plos Global Public Health, Vol: 5Epidemiological studies show a global increase in asthma, straining healthcare systems in low- and middle-income countries. There are multiple barriers to accessing diagnosis and treatment in Sub-Saharan African countries like Kenya and Sudan such as healthcare infrastructure, diagnostic tools, healthcare workers’ capacities, and cost. Asthma can be well controlled using safe and cost-effective treatments such as inhalers. Stigma related to asthma negatively impacts treatment-seeking and adherence in higher-income settings, with limited information about such impacts in Sub-Saharan Africa. We conducted qualitative interviews and Focus Group Discussions in Kenya and Sudan to explore health systems aspects of diagnosis and management of chronic respiratory diseases. Participants included patients, primary care healthcare workers, hospitals, and community actors. Data were analysed through a framework approach; our initial analysis showed that asthma stigma was prevalent in both countries. Further analysis was using the Health, Stigma, and Discrimination Framework by Stangl. Negative perceptions about the aetiology and prognosis of asthma contribute to stigma. Anticipated, internalized stigma, and enacted stigma affects individuals with asthma, encouraging them to hide their symptoms and resist diagnosis. This contributes to delayed healthcare seeking and treatment uptake, impacting both individuals with asthma and health professionals. Overall, stigma exacerbates challenges in communicating diagnosis, managing the illness, and maintaining psychosocial health and well-being for those with asthma. Poor asthma control can exacerbate fear and stigma. Improving asthma control has the potential to reduce fear and positively influence community norms. The rollout of inhalers and spacers for asthma treatment should be accompanied by deliberate stigma reduction strategies and awareness raising at all levels of the system.
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Journal articleMueller A, Wouters E, Burney P, et al., 2025,
Quality of life associated with breathlessness in the multinational Burden of Obstructive Lung Disease (BOLD) study: a cross-sectional analysis
, Pulmonology, Vol: 31, ISSN: 2531-0429IntroductionEvidence of an association between breathlessness and quality of life from population-based studies is limited. We aimed to investigate the association of both physical and mental quality of life with breathlessness across several low-, middle- and high-income countries.MethodsWe analysed data from 19 714 adults (31 sites, 25 countries) from the Burden of Obstructive Lung Disease (BOLD) study. We measured both mental and physical quality of life components using the SF-12 questionnaire, and defined breathlessness as grade ≥2 on the modified Medical Research Council scale. We used multivariable linear regression to assess the association of each quality-of-life component with breathlessness. We pooled site-specific estimates using random-effects meta-analysis.ResultsBoth physical and mental component scores were lower in participants with breathlessness compared to those without. This association was stronger for the physical component (coefficient = −7.59; 95%CI −8.60, −6.58; I2 = 78.5%) than for the mental component (coefficient = −3.50; 95%CI −4.36, −2.63; I2 = 71.4%). The association between physical component and breathlessness was stronger in high-income countries (coefficient = −8.82; 95%CI −10.15, −7.50). Heterogeneity across sites was partly explained by sex and tobacco smoking.ConclusionQuality of life is worse in people with breathlessness, but this association varies widely across the world.
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Journal articleShaaban FL, Groenendijk RW, Baral R, et al., 2025,
The path to equitable respiratory syncytial virus prevention for infants: challenges and opportunities for global implementation
, The Lancet Global Health, Vol: 13, Pages: e2165-e2174, ISSN: 2214-109XThe approval for a respiratory syncytial virus (RSV) maternal vaccination programme by Gavi, The Vaccine Alliance, marks substantial progress toward equitable access, with important work still to come. Several countries, most of which are high-income, have introduced RSV immunisation either using a vaccine containing the RSV fusion protein in its prefusion conformation, which is given to pregnant people in late pregnancy, or by using a long-acting monoclonal antibody (mAb) administered directly to infants. Post-implementation real-world effectiveness data show a major impact in reducing medically attended RSV-lower respiratory tract illness and hospitalisation using either strategy. Although RSV poses a substantial burden to infants and vulnerable children worldwide, 97% of associated mortality occurs in low-income and middle-income countries. However, few of these countries have authorised and introduced RSV preventive strategies. This Review outlines the challenges and opportunities for expanding access to RSV prevention for infants in resource-restricted settings guided by WHO's Immunization Agenda 2030 and the UN's Leave No One Behind framework for non-discriminatory sustainable development. We discuss burden, vaccine and mAb development, health economics and impact modelling, policy, implementation and programmatic considerations, surveillance, and awareness as key RSV domains. This Review summarises recent advances in research and highlights the urgent steps needed to ensure equitable access to RSV prevention for all infants worldwide.
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Journal articleAli N, Katsouli J, Auyang E, et al., 2025,
Microplastic and nanoplastic pollution and associated potential disease risks
, The Lancet Planetary Health, Vol: 9, ISSN: 2542-5196Microplastics and nanoplastics (MNPs) are emerging pollutants widely dispersed in the environment, with humans primarily exposed through ingestion and inhalation. Although their biological effects are being increasingly studied, their potential effect on human health and disease risk remains uncertain. This Review summarises evidence on potential disease risks of human exposure to MNPs, while highlighting key limitations and research gaps. Evidence suggests that MNP exposure might elevate the risk of various diseases, including metabolic, respiratory, cardiovascular, neuroendocrine, hepatic, renal, and skin disorders, as well as infectious diseases, cancer, and ageing-related disorders. Despite extensive evidence of adverse effects in animal models and cell cultures, direct evidence linking MNP exposure to human disease risk remains scarce. A key challenge on research of MNPs lies in the scarcity of robust human exposure data and the narrow scope of existing studies on specific types of MNPs, leaving several environmentally prevalent plastic particles understudied. Addressing these gaps will require investigating the mechanisms of toxicity, relevant biomarkers, and disease pathways associated with MNP exposure. Such efforts will be essential to clarify human health risks and inform future regulatory and mitigation strategies.
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