Pulmonary sarcoidosis and asthma can present identical symptoms, making clinical evaluation difficult if the two diseases overlap. Diagnostic challenges often lead to either overdiagnosis of asthma in patients with confirmed sarcoidosis or withholding appropriate asthma treatment. The true prevalence of patients with bronchial hyperresponsiveness, the hallmark of asthma, among sarcoidosis patients remains unknown, although it is suspected to be significantly higher compared to the general population. Therefore, a positive bronchial challenge test, often considered crucial for confirming asthma in symptomatic individuals with normal spirometry, should not be regarded as decisive in patients with pulmonary sarcoidosis. However, the coexistence of both diseases is possible and should always be considered. Caution is advised as patients prematurely and incorrectly diagnosed with asthma are exposed to unnecessary medical costs and lifelong treatment. Nevertheless, inhaled glucocorticosteroids and bronchodilators may be temporarily used in sarcoidosis patients because of their beneficial effect on symptom control, regardless of a concurrent asthma diagnosis. Despite the existing evidence that patients with sarcoidosis can develop asthma and atopy, the complex cellular pathways and genetic predispositions involved in the pathogenesis of both diseases remain largely unknown. To address these issues in clinical practice, the article aims to discuss the mechanisms involved in the etiopathogenesis of asthma and sarcoidosis and to analyze the available diagnostic and therapeutic methods relevant to both conditions.

To investigate whether iron metabolism exerts a causal influence on chronic rhinosinusitis (CRS) and to identify iron-related biomarkers and regulatory genes with diagnostic and therapeutic potential.

A two-sample Mendelian randomization (MR) analysis was conducted using large-scale GWAS summary statistics for four iron-related traits and three nasal inflammatory diseases. Significant SNPs were mapped to proximal genes and analyzed via Gene Ontology (GO), KEGG pathway enrichment, and protein-protein interaction (PPI) network construction. Candidate gene expression was validated using the GSE69093 transcriptomic dataset and qRT-PCR in nasal mucosal tissues from CRS patients and healthy controls. Molecular docking simulations were performed to assess ligand interactions, and clinical association and machine learning models were applied to evaluate diagnostic relevance and predictive performance.

MR analysis identified transferrin saturation (TSAT) as a causal protective factor for CRS (OR = 0.9988, P = 0.014). Thirty-one genes were mapped from MR-associated SNPs, with SLC17A4 highlighted as a key candidate gene. Enrichment analysis indicated involvement in iron metabolism and inflammatory regulation. SLC17A4 expression was significantly downregulated in both GSE69093 and clinical qRT-PCR samples. TSAT and SLC17A4 levels showed strong inverse correlations with Lund-Mackay and SNOT-22 scores. Molecular docking identified Troglitazone as a strong-binding ligand to SLC17A4 (-10.0 kcal/mol). Machine learning models integrating iron biomarkers and SLC17A4 expression achieved high discriminative performance (AUC = 0.828-0.849) and demonstrated good calibration and net clinical benefit according to calibration and decision curve analyses, supporting their potential clinical applicability.

TSAT confers protective effects in CRS, and SLC17A4 represents a promising biomarker and therapeutic target. The integrative strategy combining causal inference, transcriptomic validation, molecular docking, and machine learning modeling links iron homeostasis to CRS pathophysiology and demonstrates translational potential through clinically applicable predictive models.

Despite decades of research, HIV-1 continues to infect millions annually, underscoring the urgent need for a safe and effective vaccine to curb the ongoing global pandemic. Among the many strategies explored, viral vectors have been the most intensively studied, with adenoviral and poxviral platforms serving as the leading approaches. These vectors have advanced through extensive preclinical evaluation and multiple large-scale clinical trials, demonstrating safety and the ability to induce cellular and humoral responses. Yet, they have also revealed key challenges, including pre-existing vector immunity, limited durability of responses, and in some cases, increased susceptibility to infection. Importantly, these trials clarified the limitations of Env-focused immunity, highlighted the value of heterologous prime-boost regimens, and reinforced the dual need for broadly neutralizing antibodies and functional T cell responses. While vector-based COVID vaccines achieved protective efficacy, lessons learned from adenoviral and poxviral efforts continue to shape the field, directly informing the design of next-generation platforms such as mRNA and engineered viral vectors.

Choroid plexus (ChP) enlargement is a neuroimaging biomarker of neuroinflammation and neurodegeneration. However, evidence of ChP structural and perfusion alterations in long coronavirus disease (COVID) and their clinical relevance remains limited.

This study included 86 long COVID, 67 recovered COVID, and 26 COVID-negative healthy controls (HCs). ChP volume and cerebral blood flow (CBF) were quantified, and their associations with Alzheimer's disease (AD) symptoms and plasma biomarkers were examined.

Both patient groups showed higher ChP volume and lower CBF than HC. Relative to recovered COVID, long COVID patients had a larger ChP volume, but no significant difference in CBF. ChP volume correlated positively with glial fibrillary acidic protein (r = 0.35) and phosphorylated tau217 (p-tau217; r = 0.54), while CBF correlated negatively with p-tau217 (r = -0.56). Both ChP volume and CBF were associated with cognitive decline measured with Mini-Mental State Examination and Clinical Dementia Rating.

These findings suggest that ChP differences in long COVID are associated with AD-related cognitive decline and increased plasma biomarkers.

Long coronavirus disease (COVID) patients show choroid plexus (ChP) enlargement and reduced cerebral blood flow. ChP alterations are associated with Alzheimer's disease (AD)-related symptoms and plasma biomarker changes. ChP alterations on magnetic resonance imaging may serve as imaging markers for tracking neurological symptoms and AD-related pathology in post-COVID patients.

Human TMPRSS2 is a type II transmembrane serine protease and an essential host factor for SARS-CoV-2 and influenza A virus (IAV H1N1) infections. It facilitates the cleavage of viral surface glycoproteins, which are required for membrane fusion. This importance makes it an attractive target for host-directed antiviral therapies. We previously identified N-0385 and N-0920 as nanomolar TMPRSS2 inhibitors and demonstrated their antiviral potency against several SARS-CoV-2 variants. Here, we screened another twelve N-0385/N-0920 analogs with improved pharmacokinetics. Compounds 9 and 10 showed strong inhibition of TMPRSS2 activity and viral entry: they blocked pseudoviruses and authentic SARS-CoV-2 JN.1 and IAV H1N1 in Calu-3 cells. Compound 9 displayed a synergistic effect with baloxavir during IAV H1N1 infection. Both compounds highly reduced H1N1 infection in air-liquid interface cultures and mouse models, thus highlighting their broad antiviral potential. The discovery of broad-spectrum, host-directed antivirals against current and emerging human viruses is critical in preparing for future pandemics.

A localized pertussis outbreak involving 10 unvaccinated infants occurred in Kumamoto, Japan, during March-May 2025. Nine infants were admitted to the pediatric intensive care unit, 6 of whom received a confirmed diagnosis of macrolide-resistant Bordetella pertussis infection. This outbreak highlights the importance of booster vaccinations and resistance surveillance.

We report the emergence and spread of multilocus variable-number tandem-repeat analysis type 27 (MT-27) macrolide-resistant Bordetella pertussis (MRBP) in Kobe, Japan, in 2025. Whole-genome sequencing revealed that MT27-MRBP did not originate from the widely circulating MT27 macrolide-sensitive B. pertussis in Japan but was closely related to MRBP in China.

The Minnesota Department of Health identified an outbreak of Legionnaires' disease in a city in northern Minnesota, USA, in April 2023 that continued until chloramine disinfection of the community water system was implemented. Before chloramine disinfection was implemented, Legionella pneumophila was detected in 1 of 16 samples from the drinking water distribution system and in 5 of 10 premise plumbing samples using both cultivation-dependent (Legiolert) and cultivation-independent (digital PCR) assays in this independent investigation. Approximately 11 weeks after disinfection was implemented, all distribution system samples tested negative; however, 1 of 6 Legiolert-tested and 3 of 6 digital PCR-tested premise plumbing samples were positive. After 24 weeks of disinfection, all samples collected from the distribution system and premise plumbing tested negative. Our results show that a community water system supplied by groundwater supported substantial growth of L. pneumophila in premise plumbing and that chloramine disinfection halted the outbreak.

We evaluated the efficiency of SARS-CoV-2 detection from patient respiratory specimens by comparing 3 cell lines: Vero E6, Vero E6 expressing transmembrane protease serine 2 (Vero E6 T2), and Vero E6 expressing angiotensin-converting enzyme 2 and transmembrane protease serine 2 (Vero E6 A2T2). We compared a range of sample types, clinical conditions, and real-time reverse transcription PCR cycle threshold values. Vero E6 A2T2 exhibited enhanced sensitivity by supporting efficient virus entry and replication with faster cytopathic effect. Vero E6 culture isolated infectious virus only up to 3 days after PCR confirmation but with Vero E6 A2T2 cells, culture occurred up to 7 days after confirmation. Whole-genome sequencing showed no evidence of adaptive mutations when Vero E6 A2T2 was used for viral culture, supporting use for downstream analyses. Optimized infectious virus detection systems are needed for research and clinical settings, particularly for high-risk, immunocompromised populations that produce virus longer and contribute to variant emergence.

Fungi in the family Trichosporonaceae are rarely involved in invasive disease but are frequently associated with colonization or respiratory allergic infection. Trichosporonaceae exhibit intrinsic resistance to echinocandin antimicrobial drugs, posing challenges for treatment and contributing to high mortality rates. We complied a nationwide analysis of 112 cases of invasive disease caused by Trichosporon spp. and related fungi, diagnosed in France over 20 years, that combined clinical data, susceptibility profiles, and molecular identification. We identified 12 species; T. asahii was the most common species recovered, and the new species T. austroamericanum was next. Comparison of clinical data highlighted species and genotypic differences, such as a much higher proportion of children infected by T. asahii and major differences in antimicrobial drug susceptibility. Correct identification is not only of epidemiologic interest but also necessary for patient management because of the varying clinical and microbiological characteristics found in different species.