Historically endemic to parts of South America, Oropouche virus (OROV) has caused an estimated 500,000 infections since its discovery, with a marked geographic expansion beyond the Amazon basin into other regions of South America and the Caribbean since late 2023. This Review synthesises current evidence on OROV epidemiology, transmission dynamics, clinical manifestations, diagnostics, viral diversity, and public health impact, with the primary objective of identifying critical knowledge gaps and outlining priorities for surveillance, research, and control. Human transmission occurs primarily via Culicoides paraensis midges, while the competence of other vectors, the role of animal reservoirs in sustaining sylvatic transmission, and the contribution of vertical and sexual transmission remain incompletely understood. Although most infections are self-limiting, reports of neurological disease, Guillain-Barré syndrome, adverse pregnancy outcomes, and rare fatalities highlight uncertainties regarding pathogenicity, risk factors for severe disease, and long-term sequelae. The known teratogenicity of related Simbu serogroup orthobunyaviruses in animals further raises concerns about foetal risk in humans. Environmental change, expanding vector ranges, and viral evolution are likely contributing to outbreak emergence and geographic spread. Based on the available evidence, this review highlights priority gaps in epidemiological surveillance, diagnostics and genomic monitoring, vector competence and ecology, transmission pathways, and countermeasure development. Addressing these gaps through coordinated surveillance, improved laboratory capacity, targeted vector control, and focused research will be essential to mitigate the public health impact of OROV and reduce the risk of further spread.

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic interstitial lung disease characterized by aberrant extracellular matrix (ECM) remodeling, epithelial dysfunction, and limited therapeutic options. Genetic studies implicate Desmoplakin (DSP), a desmosomal adhesion protein, in IPF susceptibility; however, its mechanistic role remains unclear. This study aimed to investigate the role of DSP in regulating fibrotic and ECM remodeling pathways in alveolar epithelial cells. DSP was silenced using siRNA in adenocarcinoma-derived human alveolar epithelial A549 cells. DSP loss induced epithelial-to-mesenchymal transition, enhanced cell migration, and increased epithelial permeability, along with upregulation of fibrotic and ECM-associated genes. Pathway enrichment analysis of DSP interactors (STRING database) identified the Wnt/β-catenin signaling as a potential key pathway. Mechanistic validation using cycloheximide chase assays, qPCR, western blotting, immunofluorescence, and luciferase-reporter assays suggested that DSP loss destabilizes desmosomal complexes, promoting plakoglobin (γ-catenin) degradation while reducing β-catenin turnover. This was associated with increased nuclear accumulation of β-catenin and enhanced TCF/LEF-dependent transcription, leading to elevated expression of ECM-related genes, including COL1A1 and MMP9. DSP overexpression suppressed Wnt/β-catenin signaling and fibrotic gene expression, while pharmacological inhibition of this pathway attenuated DSP-dependent increases in ECM-associated gene expression. These findings suggest that DSP may function as a regulator of alveolar epithelial homeostasis and extracellular matrix remodeling in an in vitro epithelial model. Loss of DSP is associated with activation of Wnt/β-catenin-mediated fibrotic signaling, correlating with reduced plakoglobin stability. This study provides mechanistic insight into epithelial-matrix crosstalk in vitro and identifies a candidate pathway that may contribute to ECM dysregulation in IPF, the disease relevance of which will require validation in primary human alveolar epithelial cells and in vivo models.

National AI health strategies are proliferating, yet development methodologies remain largely undocumented, limiting collective learning. India's Strategy for AI in Healthcare (SAHI) was developed through a three-phase participatory process spanning situational analysis, regional consultations across four geographic zones, and structured synthesis engaging over 300 stakeholders. Documenting that process architecture for examination and adaptation by other countries is the methodological contribution of this paper. Consultation surfaced five system-level constraints recurring across emerging AI health ecosystems and drove a fundamental restructuring from prescriptive implementation planning to an enabling framework. A dual framework emerged separating technical prerequisites from governance and implementation conditions, with equity embedded as an operational requirement throughout. Rights-based regulation, market-led innovation, and state-centric control have dominated global AI governance debate. SAHI reflects a fourth approach, anchoring governance in shared digital public infrastructure rather than rules alone, and offers a distinct reference point for any country developing a health-specific AI strategy.

Human cases of Middle East respiratory syndrome coronavirus (MERS-CoV) have declined in recent years, but continued surveillance and research is needed to understand this trend and mitigate future zoonotic threats.

Large national, integrated biobanks have revolutionized how genetics-linked healthcare data can be scaled, providing access to massive databases to researchers globally. Recognizing the importance of integrated biobanks for public health and national scientific advancement, countries around the world have launched similar initiatives. Despite comprising a quarter of the world's population, South Asia accounts for only 1·8% of EHR-indexed publications and 0·2% of GWAS participants. We argue for a South Asia Biobank Consortium: (1) a regional governing body overseeing interoperability across (2) national-level integrated biobanks that adapts the UK Biobank model to regional contexts (3) supported by federated analytics infrastructure with global access. If enacted, the consortium represents a scientific imperative and a pathway to digital health equity for nearly two billion people living in South Asia. We present a framework based on hallmarks of successful integrated biobanks and critical success factors. We propose a timeline for its establishment. Without decisive action, current disparities will worsen, leaving South Asia's population marginalized as the transformative revolution continues. With a federated, equitable strategy, South Asia can transform from a peripheral participant into a central driver of biomedical discovery - strengthening health systems, advancing equity, and realizing the global promise of precision medicine.

Background and objectives While some studies suggest that lower birth weight is associated with poorer adult lung function, findings regarding early childhood, adolescent, and adult growth variables remain inconsistent. We conducted this study to determine whether low lung function in Indians is related to lower birthweight and early growth. Methods The New Delhi Birth Cohort (NDBC) was used as the study population to examine patterns and periods of growth in infancy, childhood, and adolescence using a conditional growth model. Lung function data were collected using spirometry and the forced oscillation technique at approximately 50 yr of age. We further examined associations of conditional size measures with adult lung function outcomes using multiple linear regression models. Results Lung function was positively associated with weight till 5 yr of age. Further, an increase of 1 standard deviation (SD) in conditional weight between 5-10 yr resulted in a decrease in forced vital capacity (FVC) of 50 mL [95% confidence interval (CI) -0.10 to 0.00 ( P = 0.08)]. Between 10-50 yr of age, a negative association was observed between weight and lung function. Positive associations of some of the measures of lung function were observed with length at birth, 2 yr, adolescent height, and final adult height. An increase of 1 SD in conditional height between birth and two years resulted in an increase in forced expiratory volume in 1 second (FEV1) of 130 mL (95% CI, 0.09 to 0.17). Interpretation and conclusion Birth weight and birth length, and greater than predicted linear growth throughout childhood, are independently associated with better adult lung function, in terms of spirometry and oscillometry. It is plausible that greater than predicted weight gain after 5 yr of age or during adolescence, or adulthood has an inverse association with lung function.

Asthma and chronic obstructive pulmonary disease (COPD) have many common clinical characteristics, thus making reliable differentiation between these two challenging. The goal of this study is to determine the clinical value of exhaled breath condensate (EBC) derived miRNAs to discriminate between asthma and COPD. This cross-sectional study included 65 subjects each with asthma (mean/SD age: 39/13 years, Malen/%: 27/42%), COPD (mean/SD age: 61/9 years, Malen/%: 53/81%) and healthy controls (mean/SD age: 34.4/12 years, Malen/%: 50/77%). EBC was collected using R-tubes and 40 EBC samples from each group were used for miRNA profiling. Profiling data was curated and the most highly expressed miRNAs were shortlisted for further validation. Selected microRNAs were subsequently validated using quantitative-PCR in an independent set of 25 subjects from both disease groups. A total of 103 miRNAs were significantly upregulated in the EBC of asthma patients and 97 miRNAs were upregulated in the EBC of COPD patients compared to control group. However, miR-512-3p was downregulated and miR-517c was upregulated in COPD compared with asthma. The top unique miRNAs were shortlisted for further validation. Of these, miR-375 was upregulated in asthma, while miR-297, miR-367 and miR-539 were upregulated in COPD compared with healthy controls. Further, miR-512-3p was down-regulated and miR-517c was upregulated in COPD compared with asthma. The comparison exhibited excellent discriminatory power with 100% differential expression of miR-512-3p and miR-517c secreted by respiratory cells, they could be quantitated in EBC samples and used to differentiate between asthma and COPD.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic and progressive liver disease with an increasing global burden that starts with an early stage of simple steatosis (MASL) which frequently progresses to liver cirrhosis and hepatocellular carcinoma (HCC). Despite its widespread occurrence, the MASL or steatotic stage, characterized by excessive fat accumulation in the liver and considered reversible and benign, has not been extensively studied. To study MASL effectively, it is imperative to have a clinically relevant model system that focuses solely on steatosis, in a progressive and time-dependent manner, recapitulating molecular changes associated with human disease. We established a chronic cellular model of MASL using a primary immortalized human hepatocyte cell line treated with a low dose mixture of fatty acids. This model mimics the pattern of chronic disease progression, shows minimal lipotoxicity, exhibits progressive lipid accumulation (from early to moderate steatosis), and demonstrates macrosteatosis, a hallmark of MASL. To determine whether this model recapitulates both morphological and molecular aspects of steatosis, we measured the expression of key genes and pathways found to be dysregulated in a recently available early MASL patient dataset as well as a non-human primate model of MASL. In support of the relevance of our model, we observed increased fatty acid uptake, lipogenesis, mitochondrial activity, metabolic rewiring, and autophagic alterations that significantly overlap with the pathological features of human and non-human primate MASL. In conclusion, we generate a relevant cellular model of steatosis that can serve as a robust platform for screening of existing chemical libraries to identify potent inhibitors of MASL as well as discovering novel therapeutic targets by mechanistically studying altered molecular signatures associating early stages of MASLD.

INTRODUCTION:This network meta-analysis (NMA) of randomized controlled trials (RCTs) aimed to evaluate the efficacy and safety of pharmacotherapies for progressive fibrotic-interstitial lung diseases (PF-ILDs) to identify optimal treatments. METHODS:We searched for RCTs on PF-ILD [idiopathic pulmonary fibrosis (IPF), connective tissue disease-ILD (CTD-ILD), chronic hypersensitivity pneumonitis (CHP), and pulmonary sarcoidosis] pharmacotherapies until 5 June 2025. NMA assessed efficacy [forced vital capacity, diffusing capacity of lungs for carbon monoxide, 6-minute-walk distance] and safety [serious adverse events (SAEs) and all-cause mortality] (PROSPERO: CRD42024554475). RESULTS:We included 65 studies (13,521 participants) for 48 drugs in IPF, 10 studies (1,508 participants) for eight drugs in CTD-ILD, four studies (259 participants) for three drugs in CHP, and nine studies (525 participants) for nine drugs in pulmonary sarcoidosis. In IPF, pirfenidone, nintedanib, and IFNγ-1b slowed lung function decline and reduced mortality. In CTD-ILD, pirfenidone, nintedanib, tocilizumab, and cyclophosphamide improved lung function and reduced mortality, with higher SAEs for nintedanib and cyclophosphamide. Pirfenidone and prednisolone benefited CHP, while budesonide improved lung function in pulmonary sarcoidosis. CONCLUSIONS:Anti-fibrotic drugs - Pirfenidone and nintedanib effectively slow disease progression and reduce mortality in PF-ILDs. Emerging therapies like IFNγ-1b warrant further research, underscoring the need for large, high-quality RCTs.

BACKGROUND AND AIM:Pulmonary sarcoidosis and pulmonary tuberculosis (PTB) are two granulomatous diseases with similar clinical presentations. This study explored the potential of microRNAs (miRNAs) in exhaled breath condensate (EBC) as non-invasive diagnostic biomarkers to distinguish between pulmonary sarcoidosis and PTB.  Methods: EBC samples were collected from 46 participants (20 with PTB, 26 with pulmonary sarcoidosis) and 20 healthy controls and miRNA profiling was done. Differentially expressed miRNAs were further validated using qRT-PCR in independent cohorts in EBC (17 PTB, 18 sarcoidosis, and 25 controls) and blood (10 PTB, 10 sarcoidosis, and 10 controls).  Results: Initial profiling identified 19 miRNAs differentially expressed between pulmonary sarcoidosis and PTB, one between sarcoidosis and controls, and 22 between PTB and controls. The top five upregulated miRNAs (miR-132, miR-362-5p, miR-181c, miR-181a, and miR-512-3p) and two downregulated miRNAs (miR-454 and miR-139-5p) in sarcoidosis compared to PTB were selected for validation. Validation showed significant downregulation (p value <0.05) of only miR-454 in EBC of sarcoidosis patients compared to PTB patients with an optimal AUC of 0.663. miR-150* discriminated sarcoidosis patients from healthy controls with an AUC of 0.982. When PTB were compared to healthy controls, miR-454 and miR-139-5p were discriminating both groups with AUCs of 0.991 and 0.994 respectively in EBC. CONCLUSIONS:These findings suggest that while miR-454 differentiated pulmonary sarcoidosis from pulmonary tuberculosis, their clinical utility in EBC is limited. Further investigation is needed to explore their diagnostic potential, and to improve diagnostic accuracy in EBC.

We propose a new nomenclature for mpox virus lineages with sustained human-to-human transmission to improve tracking, communication and public health response.

The "Investigating and translating genomic evidence for public health response to SARS-CoV-2 (INSIDE SARS-CoV-2)" project is part of the initiative "Joint science and technology cooperation call for joint project proposals for the years 2021-2023" promoted by the Italian Ministry of Foreign Affairs and International Cooperation (MAECI) and the Republic of India. To start the project activities, the pandemic response and the epidemiological situation in Italy and in India, together with the genomic surveillance strategies for SARS-CoV-2 virus in the two countries, are here described.