The development of novel antiviral nanomaterials is an important approach for addressing emerging viral threats. In this study, glycyrrhizic acid-modified gold nanoparticles (GA-Au NPs) were successfully synthesized and characterized, and their inhibitory effects against porcine reproductive and respiratory syndrome virus (PRRSV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pseudovirus were systematically evaluated. At non-cytotoxic concentrations, GA-Au NPs showed inhibitory activity against PRRSV in vitro. Stage-specific assays suggested that intracellular replication-related events were prominently affected, with additional inhibitory effects observed during adsorption, invasion, and release, whereas no direct virucidal activity was detected under the tested conditions. Furthermore, GA-Au NPs dose-dependently reduced SARS-CoV-2 pseudovirus infection-associated reporter signals in HEK-293T-ACE2 cells, supporting inhibitory activity in an additional viral model. In conclusion, GA-Au NPs represent a biocompatible antiviral nanomaterial with multi-stage inhibitory activity against PRRSV and inhibitory effects in a SARS-CoV-2 pseudovirus model, supporting their further evaluation as antiviral nanomaterials in enveloped virus-related models.

SARS-CoV-2 continues to cause recurrent waves in the post-pandemic period, yet genomic data from Southeast Asia remain limited for several emerging Omicron lineages, including NB.1.8.1. In this study, routine acute respiratory infection (ARI) surveillance performed in Bangkok, Thailand, from January to December 2025 was integrated with real-time RT-PCR testing and complete spike-gene sequencing for lineage assignment and evolutionary analysis. Among 4756 ARI specimens, 473 (9.9%) tested positive for SARS-CoV-2. Positivity increased in late April, peaked in May (epidemiological week 21; 58.4%), and declined through late June. Lineage typing was successful for 165/473 positive samples (34.9%), identifying 16 Pango lineages. Early 2025 showed heterogeneous circulation, including XEC- and XEC.8-related lineages, whereas NB.1.8.1 predominated during the main wave, accounting for 92.4% of typed cases in May and 89.8% in June. No recombination signals meeting predefined criteria were detected in the spike dataset. The mean spike substitution rate was estimated at 1.11 × 10^-3 substitutions/site/year (95% HPD, 9.13 × 10^-4-1.31 × 10^-3), and the major Thai-containing NB.1.8.1 clade had an estimated tMRCA of 17 July 2024. These findings show that routine ARI surveillance combined with spike-based genomics can provide timely insights into SARS-CoV-2 circulation, lineage replacement, and ongoing viral evolution in Thailand.

SARS-CoV-2 is the etiological agent responsible for COVID-19. While most research has focused on structural proteins, the accessory protein Open Reading Frame 8 (ORF8) has attracted attention for its role in immune evasion and the induction of a cytokine storm. Although the exact mechanisms underlying viral pathogenicity remain to be elucidated, oxidative stress has been proposed as a key contributing factor. In this study, we evaluated the effect of intranasal administration of ORF8 on arterial blood pressure and the antioxidant system in different organs of male BALB/c mice at 2- or 8 weeks post-administration. A significant increase in blood pressure and renal total antioxidant capacity was observed in the 8-week group, and decreased catalase activity in the prefrontal cortex was observed in the 2-week group. These findings suggest that ORF8 may contribute to long-term renal alterations and potentially to mechanism relevant to cognitive dysfunction associated with COVID-19.

Pregnancy represents a distinct immunological and physiological state that modifies maternal susceptibility to SARS-CoV-2 and influences the clinical and biological course of COVID-19. Accumulating evidence indicates that the interaction between viral entry determinants, gestation-specific immune modulation, placental endocrine-angiogenic pathways, and systemic inflammatory responses underlies the characteristic manifestations of SARS-CoV-2 infection during pregnancy. This review consolidates current understanding of SARS-CoV-2 viral structure, receptor biology, and the gestational regulation of key entry cofactors, including ACE2, TMPRSS2, NRP1, CTSL and FURIN, within reproductive and placental tissues. The review further integrates documented mechanisms of cytokine-mediated immune dysregulation, endothelial injury, thrombo-inflammation, and steroidogenic alteration observed in affected pregnancies, and examines their contribution to placental malperfusion, preeclampsia-like presentations, fetal growth abnormalities and preterm birth. Published molecular and computational studies characterising trophoblast antiviral defenses, receptor expression patterns, and structural determinants of Spike-ACE2 affinity are synthesised to contextualise the biological basis of placental susceptibility and the rarity of confirmed transplacental transmission. Current evidence on maternal clinical outcomes, fetal and neonatal consequences, vaccination efficacy, therapeutic considerations and contemporary management guidelines is also critically reviewed. By integrating molecular, immunological, pathological and clinical insights, this article provides a comprehensive framework for understanding the interaction between SARS-CoV-2 infection and pregnancy-specific physiology, with implications for risk assessment, preventive strategies and maternal-fetal care.

The continuous emergence of SARS-CoV-2 variants highlights the need for novel antiviral agents with favorable safety profiles. Marine microalgae constitute a valuable source of bioactive compounds, including antiviral peptides. Building on previous in silico identification of peptides derived from the marine microalga Phaeodactylum tricornutum with predicted activity against SARS-CoV-2, this study evaluated the antiviral capacity of peptide fractions generated by enzymatic hydrolysis and separated by molecular weight (10-30, 5-10, 3-5, and <3 kDa) in human alveolar epithelial A549 cells infected with the SARS-CoV-2. Cytotoxicity analyses, assessed using MTT and resazurin assays, revealed a moderate, concentration-dependent reduction in metabolic activity while maintaining overall cell viability within an acceptable range for antiviral evaluation, with higher-molecular-weight fractions (10-30 and 5-10 kDa) displaying the most stable profiles. Antiviral activity was assessed by flow cytometry following post-infection treatment. Lower-molecular-weight fractions (3-5 and <3 kDa) showed early reductions in infection at low concentrations but exhibited variable responses. In contrast, the 10-30 and 5-10 kDa fractions showed more robust, dose-dependent inhibition at medium and high concentrations, reducing infection levels to levels close to those observed in uninfected controls. Comparative analysis with the reference antiviral drug lopinavir demonstrated that peptide fractions exhibit lower cytotoxicity while retaining antiviral activity under equivalent experimental conditions. Overall, these results indicate that antiviral efficacy is strongly influenced by peptide molecular weight and consistency of response. This work provides experimental in vitro validation of P. tricornutum-derived peptide fractions as marine antiviral candidates and supports the integration of in silico and functional approaches for marine drug discovery.

Idiopathic pulmonary fibrosis (IPF) is characterised by progressive parenchymal remodelling, driven by epithelial dysfunction, fibroblast activation, and altered immune regulation within the distal lung. Alveolar macrophages (AMs) reside in a surfactant-rich environment and are specialised for continuous lipid handling, yet the significance of this metabolic role for macrophage heterogeneity and fibrotic progression has remained incompletely integrated across studies. In this review, we synthesise evidence from human lung tissue, experimental models, lipidomic analyses, and clinical investigations to place macrophage populations described in IPF-including FABP4-high homeostatic cells and SPP1-associated disease-enriched states-within a unified lipid-metabolic context. We show that macrophage heterogeneity in IPF can be understood as a variation within a core lipid-handling programme rather than the emergence of distinct macrophage lineages. Profibrotic macrophage states are characterised by altered lipid processing and signalling, including dysregulated sterol handling, lysophospholipid pathways, and eicosanoid balance, which impair surfactant turnover and contribute to fibroblast activation. Importantly, experimental and clinical data indicate that macrophage lipid-metabolic programmes remain modifiable, although definitive disease-modifying efficacy in IPF has yet to be established. Framing macrophage states within a lipid-metabolic framework provides a coherent basis for interpreting heterogeneous datasets and supports the rationale for therapeutic strategies aimed at stabilising or restoring macrophage lipid handling in fibrotic lung disease.

Pneumoconiosis remains a major occupational lung disease associated with progressive respiratory impairment, reduced functional capacity, and diminished quality of life. Non-pharmacological rehabilitation has been increasingly proposed as a supportive intervention; however, evidence regarding its effectiveness remains heterogeneous.

This study aimed to systematically review and synthesize the available evidence on the effects of non-pharmacological rehabilitation interventions on functional capacity, quality of life, and psychological outcomes in patients with pneumoconiosis.

A systematic literature search was conducted in major electronic databases and grey literature sources in accordance with PRISMA 2020 guidelines. Studies evaluating non-pharmacological rehabilitation interventions in adults with pneumoconiosis were eligible for inclusion. Outcomes of interest included functional capacity, health-related quality of life, and psychological well-being. Due to methodological heterogeneity across studies, a qualitative synthesis was performed.

Six studies met the predefined inclusion criteria and were included in the qualitative synthesis. The reviewed evidence suggests that structured rehabilitation interventions were associated with clinically meaningful improvements in functional capacity, particularly in structured rehabilitation programs, most consistently reflected by increases in six-minute walk distance exceeding established minimal clinically important differences in three studies. Improvements in health-related quality of life and selected psychological outcomes were also reported, although outcome measures and intervention protocols varied across studies. Significant improvements in exercise capacity, dyspnea severity, and health-related quality of life were reported.

Non-pharmacological rehabilitation may provide clinically meaningful benefits for patients with pneumoconiosis, based on limited and heterogeneous evidence, particularly in terms of functional capacity and quality of life. Nevertheless, the current evidence base is limited by heterogeneity in study design and outcome reporting. Further high-quality, standardized trials are needed to strengthen the evidence and guide the clinical implementation of rehabilitation programs for occupational lung diseases.

Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), are life-threatening pulmonary disorders with high mortality rates, and effective treatments are currently lacking. Secoisolariciresinol diglucoside (SDG), a plant lignan derived from flaxseed, possesses anti-inflammatory and antioxidative activities. However, the underlying mechanisms by which SDG ameliorates ALI remain incompletely understood. This study aimed to investigate whether SDG alleviates ALI by modulating the NF-κB/NLRP3 signaling pathway. For the in vivo study, ALI was induced in mice through intranasal administration of LPS. Key indicators included lung histopathological changes, wet/dry weight ratio (W/D), protein concentration in bronchoalveolar lavage fluid (BALF), oxidative stress markers (MDA, SOD, CAT), the expression of inflammatory cytokines and chemokines (IL-1β, IL-18, TNF-α, CCL2), and the level of NF-κB/NLRP3 pathway-related proteins. In vitro experiments using LPS-stimulated RAW264.7 further explored the effects of SDG on the NF-κB/NLRP3 pathway. SDG significantly mitigated LPS-induced lung histopathological damage and nasal mucosal injury, reduced lung W/D ratio and BALF protein, and suppressed oxidative stress. Moreover, SDG downregulated pro-inflammatory cytokines (IL-1β, IL-18, TNF-α) and macrophage infiltration. It also decreased the expression of N-κB/NLRP3 pathway-related proteins. In vitro experiments further confirmed that SDG inhibited the NF-κB/NLRP3 pathway. SDG effectively alleviates LPS-induced ALI through its antioxidant, anti-inflammatory, and NF-κB/NLRP3 pathway-inhibiting properties, providing experimental evidence for its potential as a therapeutic agent for ALI.

The lung, and more specifically the airway epithelium, is continuously exposed to a wide range of inhaled environmental agents. Acting as a frontline physical and biochemical barrier, the airway epithelium orchestrates early host defense mechanisms, among which immunoglobulin A (IgA) plays a central role. Long considered sterile, the healthy lung is now recognized as a complex mucosal ecosystem harboring diverse and dynamic microbial communities, including bacteria, fungi, viruses, and archaea. Although the lung microbiome is generally transient and low in biomass, accumulating evidence suggests that it contributes to pulmonary homeostasis by supporting immune system maturation, preserving structural tissue integrity, and limiting pathogen colonization. How immune homeostasis is maintained in this constantly challenged environment remains however a central and largely unanswered question. This review synthesizes current state-of-the-art knowledge on the origin, composition, and functional determinants of the lung microbiome, with a specific focus on its bidirectional interplay with secretory IgA. We discuss microbiota-specific IgA responses, factors influencing IgA-microbiome interactions, and how these processes are disrupted in chronic and inflammatory lung diseases. Finally, we highlight major knowledge gaps and explore emerging therapeutic perspectives targeting IgA-microbiome crosstalk to restore pulmonary immune homeostasis.

The aim of this study was to examine the prevalence of Aspergillus sensitivity (AS) and allergic bronchopulmonary aspergillosis (ABPA) in children with Bronchial Asthma.

The study included 200 children with bronchial asthma. ABPA was diagnosed using Aspergillus skin testing, pulmonary function testing, absolute eosinophil count, total serum IgE, Aspergillus-specific IgE and IgG, chest radiography, and high-resolution computed tomography. Patients were diagnosed and classified according to the Rosenberg-Patterson criteria for ABPA.

Of the 200 children with bronchial asthma, 7 patients were ABPA positive. Among the ABPA-positive cases, 5 (71.4%) had uncontrolled asthma. The mean absolute eosinophil count (AEC) was significantly higher in ABPA-positive cases (418.71 ± 90.12 cells/cumm). The mean total serum IgE in positive cases was 1181.00 ± 403.42 IU/L. The mean Aspergillus-specific IgE level in positive cases was 4.74 ± 6.09 kUA/L. In ABPA-positive cases, the mean Aspergillus-specific IgG level was 26.06 ± 14.93 mgA/L.

This study demonstrated an association between ABPA and bronchial asthma in children. ABPA is a common entity in bronchial asthma and should be considered as a cause of uncontrolled asthma when symptoms persist despite the use of multiple medications.