Post-infectious bronchiolitis obliterans (PIBO) is a rare but severe chronic airway disease in children. It usually follows a severe viral lower respiratory tract infection in early life. Persistent inflammation and fibrotic remodeling of the small airways lead to narrowing, air trapping, and progressive loss of lung function. In recent years, reports from countries with high childhood infection burdens, particularly in Asia and Western countries, have drawn more attention to this condition. However, PIBO often remains under-recognized because its symptoms resemble asthma or other chronic lung diseases. This review summarizes available evidence on the epidemiology, risk factors, pathogenesis, clinical features, diagnosis, and management of PIBO in children. Literature was reviewed from published pediatric studies and case series across different regions. Several studies highlight hypoxemia and prolonged mechanical ventilation as strong predictors of disease. Recurrent viral infections, bacterial co-infections, and environmental exposures appear to increase vulnerability. The pathogenesis involves epithelial injury with neutrophildriven in ammation and fibrosis, eventually producing fixed airway obstruction. Clinically, affected children present with a chronic cough, wheeze, tachypnea, and persistent hypoxemia that do not respond to bronchodilators. High-resolution computed tomography (HRCT) is considered the most reliable imaging tool, frequently showing mosaic attenuation, bronchiectasis or air trapping. Lung function testing usually confirms irreversible obstruction. Management remains largely supportive. Systemic corticosteroids, azithromycin, and some immunomodulatory approaches have been tried with variable outcomes. What is clear is that earlier recognition and intervention can help slow progression. More collaborative research is still needed before consistent pediatric guidelines can be developed. The Journal of Ad-din Women's Medical College; Vol. 13 (2), July 2025; p 47-50

Upper respiratory tract infections (URIs) are a significant public health concern. Human behavior plays a crucial role in how often infected individuals come into contact with susceptible individuals. Among the key factors influencing the seasonality of these infections, variations in temperature and absolute humidity are critical elements driving the increase in respiratory virus infections, particularly during the winter months. Traditionally, it has been believed that cold and flu viruses thrive in winter mainly because falling temperatures lead to people spending more time indoors, which facilitates easier transmission. However, compelling evidence suggests that biological factors also contribute to the increased risk of illness in colder weather. Recent studies indicate that active mucosal defenses against bacteria extend into the mucus itself, aided by the epithelial release of antimicrobial extracellular vesicle (EV) swarms. Unfortunately, these studies have also shown that EVs are significantly weakened by exposure to cold environments.

Severe respiratory inflammation or viral infections can lead to acute lung injury (ALI), a disease characterized by diffuse inflammatory injury of the pulmonary epithelium and endothelium. Cepharanthine (CEP) is reported as a promising drug candidate due to its antiviral properties. However, CEP exhibits poor solubility and low bioavailability. Therefore, we developed a novel liposome, named CEP@LP-MCCR2, which integrates the advantages of cell membranes and lipid materials, to achieve effective accumulation of CEP in inflamed lungs. It exhibits a 1.73-fold increase in lung accumulation at 24 h in vivo, a 4.56-fold increase in cellular uptake in MLE-12 cells. CEP@LP-MCCR2 is equipped with a CCR2-overexpressed surface, enabling it to selectively neutralize elevated levels of CCL2, which is related to ALI, thereby reducing macrophage infiltration, thereby reducing the spread of inflammation, such as a reduction in levels of key pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6). CEP@LP-MCCR2 could suppress M1 macrophage polarization, which led to a marked decrease in iNOS and an increase in Arg1. It upregulated the expression of junctional proteins E-cadherin and Occludin, indicating potential recovery of the pulmonary epithelial barrier. RNA sequencing analysis implied the potential of CEP@LP-MCCR2 to inactivate the TNF/NF-κB signaling axis.

Viral respiratory infections in patients with hematological diseases over 10 years: epidemiology and impact on disease severity.

Nasal microbiome and phageome profiles are associated with prospective respiratory viral infection risk in school-aged children.

Torque teno virus (TTV) is a ubiquitous, nonenveloped DNA virus of the Anelloviridae family and a proposed surrogate marker of immune competence. Although nonpathogenic, its replication reflects host immune status and is associated with immune dysregulation during respiratory viral infections (RVIs). This study evaluated the interplay among TTV levels, inflammatory, endothelial, and coagulation biomarkers in acute RVIs. We collected 468 leftover material samples (234 respiratory and 234 blood samples) from hospitalized patients with PCR-confirmed RVIs. Patients were stratified by viral etiology, differential involvement of the respiratory tract, age, and possible co-detected pathogens. Cytokines (IL-6, IL-8, IL-1β, TNF-α), IFNs (α/β/γ), and endothelial markers (ICAM-1, VCAM-1) were quantified using microfluidic immunoassays. Routine coagulation parameters were measured in a subset of patients. TTV DNA load was quantified in both compartments using real-time PCR. Associations with inflammatory and coagulation parameters were assessed using nonparametric tests. TTV DNA was detectable across all age groups and viral etiologies, with higher levels in infants (0-1 years) and elderly patients (81-94 years). Blood and respiratory TTV levels were strongly correlated (r = 0.53, p < 0.0001). In infants, blood TTV correlated positively with IL-6 and CRP; in elderly patients, inverse correlations with TNF-α, IFN-α, and ICAM-1 suggested less regulated antiviral and endothelial responses. No significant differences were found by viral type or possible co-detected pathogens, though cytokine-TTV associations persisted. TTV levels reflect systemic and local immune activation during RVIs and deserve further investigation as possible noninvasive biomarker of immune dysregulation and thromboinflammatory risk. Longitudinal studies are needed to determine its prognostic value.

Evaluation of a novel host protein-based assay for ruling out bacterial infections in patients with suspected respiratory tract infections at an urban academic hospital.

Clinical evaluation of nasal swab specimens in VTM/UTM and RespDirect eSTM using the Panther Fusion SARS-CoV-2/Flu A/B/RSV assay.

Efficacy and safety of mirikizumab in paediatric participants with moderately-to-severely active ulcerative colitis (SHINE-1): a multicentre, open-label, non-randomised phase 2 trial.

Synergistic effects of Lactiplantibacillus plantarum GUANKE and Tryptophan on alleviating lung injury through the AHR/STAT3/IL-10 pathway in influenza infection mice.

Predictive, preventive, and personalized medicine for respiratory viral infections: Integration of mechanistic insights and precision interventions

Development of human single-domain antibodies against influenza based on NA-targeting IgG.

Seasonal Community-Acquired Respiratory Virus Infections in Patients with Cancer - Epidemiological and Clinical Overview, an Analysis of the Multicenter OncoReVir Registry.

Coronavirus disease 2019 (COVID-19) and other respiratory viral infections, such as influenza and respiratory syncytial virus (RSV), elicit both common and virus-specific host responses. Here, we present an integrative analysis leveraging the COVID-19 Host Genetics Initiative (HGI) GWAS data (freeze 7) and publicly available multi-omics datasets (including influenza/RSV human challenge transcriptomes and plasma proteomics) to construct an explainable AI model for comparing host infection mechanisms between COVID-19 and other viral illnesses. We identified shared antiviral pathways (type I interferon (IFN) signaling) active in host responses to all three viruses, as well as virus-specific mechanisms: for instance, SARS-CoV-2 infection induced uniquely strong coagulation and renin-angiotensin system dysregulation, along with sustained AP-1/MAPK activation, whereas influenza provoked more robust T-cell activation, and RSV triggered an excessive neutrophil-driven inflammatory response. Genetic risk pathway fingerprints from GWAS highlight that COVID-19 severity is associated with variants in IFN and inflammatory pathways, while host genetic effects in influenza point to distinct receptor usage (sialic acid biosynthesis) with minimal overlap. Mendelian randomization (MR) pinpointed key causal proteins for COVID-19 severity, including ABO (blood group glycosyltransferase) and inflammatory mediators, suggesting that host glycomic and immune factors modulate disease outcomes. Our explainable machine learning model integrated these multi-omic features to accurately distinguish COVID-19 from other viral infections, with SHAP interpretation confirming the predominance of the above mechanisms in model predictions. In summary, this cross-omics study provides a comprehensive comparative map of host responses in COVID-19 versus influenza and RSV, yielding biologically interpretable insights into both common antiviral defenses and unique pathogenic pathways. These findings inform the development of targeted therapies (IL-6 or MAPK inhibitors for COVID-19) and broad-spectrum antivirals (enhancing IFN responses) to mitigate severe respiratory viral diseases.

Background/Objectives: SARS-CoV-2, the causative agent of COVID-19, has been responsible for more than seven million deaths worldwide since its emergence. The Bacillus Calmette–Guérin (BCG) vaccine, used for over 100 years to prevent tuberculosis, induces a Th1-prominent immune response that is important for protection against Mycobacterium tuberculosis, other mycobacteria, and intracellular pathogens. BCG has also been shown to induce innate immune memory and heterologous protection against non-related infections. Additionally, BCG has been used as a vector to express heterologous proteins, showing protective effects against various diseases, particularly respiratory viral infections, including SARS-CoV-2. In this report, we constructed two recombinant BCG strains as potential vaccine candidates based on the receptor-binding domain (RBD) of the Spike antigen: one expressing only the RBD protein (rBCG-RBD) and another expressing the RBD protein in fusion with the LTB (Escherichia coli Labile Toxin subunit B) adjuvant (rBCG-LTB-RBD). Methods: We evaluated the induction of SARS-CoV-2-specific humoral and cellular immune responses using these vaccine candidates in a prime–boost strategy with a booster dose using the rRBD protein (produced in cell culture) and the Alum adjuvant. Antisera were evaluated for neutralization of the Wuhan and Omicron SARS-CoV-2 pseudotyped virus. Results: Either immunization scheme (rBCG-RBD/rRBD or rBCG-LTB-RBD/rRBD) induced high IgG antibody titers, with antibody neutralization against a Wuhan SARS-CoV-2 pseudotyped virus after 10 weeks. The antibody levels induced by rBCG-RBD/rRBD were maintained for up to 9 months. Interestingly, only the sera from mice receiving the prime–boost with rBCG-LTB-RBD/rRBD showed cross-reactive neutralization against the Omicron SARS-CoV-2 pseudotyped virus. Immunization with rBCG-RBD or rBCG-LTB-RBD and a rRBD booster dose promoted the induction of specific CD4+ and CD8+ T cells producing Th1/Th2 cytokines (IL-4, TNF-α and IFN-γ). Conclusions: Our study highlights the potential of the prime–boost immunization strategy using rBCG-RBD/rRBD to induce long-term immunity and rBCG-LTB-RBD/rRBD to induce cross-protection against different variants, both of which could serve as promising vaccine candidates.

This study investigates the occurrence and antimicrobial susceptibility of Bacillus spp . in pediatric patients with viral respiratory infections admitted to intensive care units. Secondary bacterial infections are known to exacerbate the severity of viral respiratory diseases and represent a major cause of morbidity and mortality during pandemics, including COVID-19. A total of 659 respiratory samples from children with respiratory symptoms hospitalized in five hospitals were analyzed. Bacterial co-infections were identified by inoculation in BHI medium and confirmed by MALDI-TOF. Antimicrobial susceptibility testing was performed using the Kirby-Bauer method, following EUCAST guidelines. Among 166 cases of bacterial co-infection, 20 (12.05%) were attributed to Bacillus spp ., with a predominance in patients infected with respiratory syncytial virus (55%). The isolates showed high susceptibility to vancomycin (85%), imipenem (80%), erythromycin (70%), and ciprofloxacin (65%). These findings reveal that Bacillus spp ., often considered an environmental contaminant, may play a clinically relevant role in pediatric viral co-infections, particularly in severe respiratory cases. This study contributes novel data to a poorly explored area of pediatric infectious disease research, emphasizing the need for routine susceptibility testing to optimize antimicrobial therapy. The results provide a foundation for future molecular studies on Bacillus spp . virulence and resistance mechanisms, supporting evidence-based management and infection control practices in critical care settings.

Persistent cough in children following viral respiratory infections is a common presentation in clinical practice, often causing concern among caregivers and prompting repeated healthcare visits. While acute viral illnesses typically resolve within two to three weeks, a subset of children experience prolonged cough that persists beyond this period, sometimes lasting up to eight weeks. The pathophysiology involves a combination of heightened cough reflex sensitivity, lingering airway inflammation, and potential involvement of coexisting conditions such as asthma or protracted bacterial bronchitis. Identifying the underlying cause can be challenging due to overlapping symptoms, variability in caregiver reporting, and the limited availability of pediatric-specific diagnostic tools. Prevalence rates vary significantly across regions, with higher incidences observed in low-resource settings where environmental exposures, overcrowding, and delayed access to care are more common. Differences in viral pathogens also influence outcomes, with viruses such as respiratory syncytial virus, rhinovirus, and adenovirus more likely to be associated with prolonged symptoms. Diagnosis relies heavily on clinical judgment, as cough characteristics and duration alone are often insufficient to distinguish between post-viral cough and more chronic respiratory conditions. Management strategies are inconsistent, with frequent reliance on medications lacking strong evidence of efficacy in pediatric populations. Antitussives, inhaled corticosteroids, and antibiotics are often prescribed without clear indications, contributing to unnecessary treatment and potential harm. Non-pharmacologic approaches, including caregiver reassurance and environmental modifications, are commonly recommended but remain under-researched. Overall, the variability in clinical practice highlights the need for more robust pediatric-focused studies and clearer guidelines to support appropriate diagnosis and treatment. Addressing these gaps is essential to improve patient outcomes, reduce unnecessary interventions, and alleviate the burden on families and healthcare systems.

Cystic fibrosis (CF), is an autosomal recessive disorder caused by mutations in the CFTR gene, leading to atypical ion transport across epithelial cells and resulting in thick mucus accumulation. This condition significantly affects multiple organ systems, particularly the respiratory and gastrointestinal tracts, leading to infections and progressive dysfunction. The introduction of CFTR modulator therapies has dramatically improved life expectancy, now reaching approximately 50 years in high-income countries. This paper presents two CF cases from the Emergency Clinical Children’s Hospital of Brașov, facing severe, life-threatening complications. One patient successfully overcame a complication related to CF, while the other experienced a significant COVID-19 complication, while presenting as a pulmonary exacerbation (PEx) of CF. The cases highlight the challenging clinical outcomes in CF and personalized approach. Intravenous antibiotic use, as piperacillin/tazobactam, one of the mainstay interventions for PEx due to its effectiveness against Pseudomonas aeruginosa, may rarely lead to severe adverse events, such as drug-induced thrombocytopenia. Furthermore, although respiratory viral infections may adversely affect pulmonary status in CF patients, emerging evidence suggests that SARS-CoV-2 infection did not severely impact this group. Paediatric inflammatory multisystem syndrome (PIMS) associated with SARS-CoV-2 infection has to be considered even in CF patients with scarce symptoms, underscoring the challenge of potential complications.

Swine influenza virus (SIV) and porcine reproductive and respiratory syndrome virus (PRRSV) are leading pathogens in pigs, whose co-infections exacerbate disease severity. Current diagnostics like RT-PCR lack suitability for rapid, on-site use, while CRISPR-based systems face challenges in convenient multiplex detection. We developed an RT-LAMP-CRISPR-Cas12a/13a-LFD dual-detection platform that integrates reverse transcription loop-mediated isothermal amplification (RT-LAMP) with the orthogonal trans-cleavage activities of CRISPR-Cas12a and Cas13a, followed by lateral flow dipstick (LFD) visualization. This assay achieved detection limits of 5 copies/µL for SIV and 2 copies/µL for PRRSV, and exhibited high specificity against other common swine pathogens. The entire process, including a 20-minute amplification at 40°C and 5-minute LFD readout, enables rapid and visual diagnosis. A preliminary validation was conducted using respiratory infection samples, demonstrating high concordance with reference methods and specificity against non-target pathogens. The RT-LAMP-CRISPR-Cas12a/13a-LFD assay provides a sensitive, specific, and potentially field-adaptable tool for the simultaneous detection of SIV and PRRSV. It is ideally suited for early screening and precise control of these pathogens in resource-limited settings.

Study on the mechanism of anti-pulmonary fibrosis action of Jingfang granules based on the Keap1-Nrf2-GPX4 pathway.