Search Results (14,729)

Background/Objectives: Concern that COVID-19 vaccination causes pulmonary nodules persists because vaccination coincided with expanded computed tomography (CT), low-dose CT (LDCT) screening, post-COVID imaging and artificial intelligence (AI)-assisted detection. This review asks whether the current literature supports causality and how vaccination history should inform thoracic imaging. Methods: A focused search of PubMed, PubMed Central and the Cochrane Library was performed through 15 July 2026. Evidence was classified as direct or contextual; no PRISMA screening, risk-of-bias scoring or quantitative synthesis was performed. Results: Direct evidence remains sparse. One case report was too confounded for inference. A two-sample Mendelian randomization study found no broad lung disease risk signal, but nodules were not modeled and the heterogeneous endpoints were exploratory. An ecological study of 1,616,750 samples linked rising detection to SARS-CoV-2 infection waves and AI-assisted reading; lacking individual vaccination data, it cannot establish whether vaccination affected detection. Screening interruption produced the opposite pattern: Lung-RADS 4 nodules rose from 8% to 29%. The most reproducible post-vaccination thoracic finding is regional lymph-node activation on [18F]fluorodeoxyglucose positron emission tomography/computed tomography ([18F]FDG-PET/CT), an expected immune response rather than a parenchymal nodule. Conclusions: Current evidence is insufficient to establish vaccination as an independent, population-level cause of pulmonary nodules. Vaccination history should guide [18F]FDG-PET/CT interpretation; CT-detected parenchymal nodules warrant standard risk stratification. Full article

Cats represent a susceptible host and a possible translational model for investigating coronavirus pathogenesis and therapeutics. Recent immunohistochemical (IHC) and histopathological studies in both human and feline tissues have demonstrated SARS-CoV-2 nucleocapsid protein (NP) and spike protein expression within pancreatic islet cells, following a classic temporal infection course. Notably, IHC analysis also reveals NP expression within exocrine ductal epithelial cells. Given that ductal epithelium functions as an islet progenitor pool during tissue injury or metabolic stress, pancreotropic coronaviruses may gain access to the endocrine compartment by exploiting this intrinsic cellular differentiation pathway. Although the precise mechanisms governing intra-islet viral entry remain to be elucidated, this review highlights the capacity of SARS-CoV-2 to compromise both the exocrine (digestive) and endocrine functions of the pancreas. Finally, we evaluate the therapeutic potential of direct-acting antivirals—specifically RNA-dependent RNA polymerase (RdRp) and protease inhibitors—as monotherapies and in synergistic combination to limit pancreatic injury and mitigate the diabetogenic effects of coronaviruses across both acute infection and post-acute sequelae, such as human long-COVID syndrome. Full article

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in substantial global morbidity and mortality since its emergence in late 2019. This retrospective study aims to determine the comorbidity patterns, co-occurrence networks, and associated demographic factors among 244 deceased COVID-19 cases in Grenada between 2021 and 2022. The prevalence of comorbid conditions varied considerably across diseases. Hypertension was the most frequently observed condition (41%) followed by diabetes (34.8%), and ARDS (27%). Our co-occurrence analysis revealed a densely interconnected core of cardiometabolic and respiratory conditions, particularly involving hypertension, diabetes, and ARDS. Stratified clustering analyses demonstrated that multimorbidity patterns were broadly consistent across gender but differed by age group and vaccination status, with older individuals showing more pronounced clustering of cardiometabolic conditions. Logistic regression analysis further identified age and gender as significant factors associated with the distribution of specific comorbidities, including higher odds of hypertension among older individuals. This study highlights the central role of cardiometabolic diseases and older age in COVID-19 mortality in Grenada in 2021–2022 and underscores the importance of multimorbidity structures rather than isolated conditions. We suggest early identification of high-risk multimorbidity profiles, particularly among older adults, to improve clinical management and preventive strategies during future infectious disease outbreaks. Full article

Population immune pressure from vaccination and prior infection continues to drive the evolution of SARS-CoV-2. Systematic characterization of RBD mutations under complex immune backgrounds is essential for understanding viral adaptation and evolutionary trajectories. Here, we applied a deep mutational scanning (DMS) to comprehensively map the neutralization escape landscape of the Omicron variant JN.1 and its descendant lineage XEC, under immune pressure from individuals who experienced Omicron breakthrough infections following three doses of inactivated vaccines. A neutralization escape map for the single amino acid substitutions in the RBD of JN.1 or XEC was generated, and the escape efficiency of each mutation was determined. The results show that RBD escape mutations are hierarchically organized: low-intensity signals are widespread, whereas high-intensity escape is confined to a few key sites. These escape mutations are not confined solely to the receptor-binding motif (RBM) but are broadly distributed across the entire RBD. Many escape sites could accommodate multiple amino acid substitutions. Integration of DMS data with genomic surveillance of circulating variants from 2024 to 2025 revealed significant overlap between experimentally identified escape sites and mutations observed in natural isolates. This overlap increased substantially in 2025, with site concordance rising from 27.17% and 26.81% to 45.09% and 47.10% for JN.1 and XEC, respectively. The natural prevalence of these escape mutations is further shaped by factors such as receptor-binding affinity, protein stability, and epistatic interactions. Overall, our findings suggest that SARS-CoV-2 antigenic evolution follows the pattern of multiple pathways within a constrained space, providing new insights into the adaptive mechanisms of Omicron-derived variants under hybrid immune pressure. Full article

Seasonal variation in SARS-CoV-2 transmissibility is difficult to estimate directly from year-round epidemic data because interventions, behavior, reporting, immunity, and viral evolution change concurrently. We therefore asked whether cross-country differences observed during the initial exponential-growth phase could be used to infer country-specific seasonal modulation. Early-pandemic basic reproduction numbers (R₀) from 118 countries were linked to 96 harmonized environmental and population-level predictors. Among nine candidate algorithms evaluated across 100 repeated train–test splits, ridge regression using the combined predictor set provided the best balance of predictive accuracy, generalization, and temporal stability. The selected model was then driven by daily climatological covariates to reconstruct annual baseline R₀(t) profiles. Predicted transmissibility generally peaked during winter in the Northern Hemisphere and approximately six months later in the Southern Hemisphere, whereas equatorial countries showed weaker or multimodal patterns. Seasonal forcing amplitude increased strongly with absolute latitude (r = 0.85; mean 0.064 across 77 temperate countries), and predicted R₀ peaks aligned more closely with minimum ultraviolet radiation than with minimum temperature. These ecological associations do not establish causality, but they provide country-specific seasonal-forcing parameters for epidemic models and a baseline environmental context for comparing early-pandemic trajectories. Full article

Vitamin D is a fat-soluble vitamin, considered a prohormone, that plays a fundamental role in calcium absorption and reabsorption, as well as the modulation of inflammatory response in infectious conditions such as COVID-19. A literature search was conducted in scientific databases and official sources, selecting studies published in the last 10 years in Spanish and English related to vitamin D and COVID-19; studies unrelated to the nutritional approach were excluded to reduce bias and ensure a rigorous and reproducible analysis. It was observed that the probability of contracting COVID-19 increases as the D3 hypovitaminosis prevalence increases. In Mexico, the relevance of vitamin D deficiency or supplementation in this disease has been controversial. Some studies claim that vitamin D supplementation could be a protective factor. According to the National Health Survey in Mexico (Ensanut), the Mexican population has significant deficiencies in this vitamin, contributing to an unfavorable diagnosis, particularly for children and pregnant women, as it is considered a deficiency in the blood when it is below 30 ng/mL and insufficiency when below 20 ng/mL, making these deficiencies important risk factors in the development of COVID-19 severe cases. Nevertheless, the use of vitamin D as an adjuvant agent in the treatment of COVID-19 can represent one of the main options for public health, providing therapeutic properties and health benefits. Full article

Coronaviruses are responsible for numerous diseases causing substantial morbidity and mortality to both humans and animals. In particular, they have caused three significant outbreaks in humans including severe acute respiratory syndrome 1 (SARS-CoV-1), Middle East respiratory syndrome (MERS-CoV), and, most recently, the severe acute respiratory syndrome 2 (SARS-CoV-2) pandemic. Two relevant veterinary diseases are porcine transmissible gastroenteritis virus (TGEV) and porcine epidemic diarrhea virus (PEDV), which cause severe losses in the pork industry. While efficacious vaccines were developed in an unprecedented timeframe for COVID-19, vaccines have not been commercialized for other human coronaviruses and vaccines against animal coronaviruses have limited efficacy and logistical challenges in administration. There is a clear need for more efficacious vaccines with simpler methods of delivery and administration for both human and veterinary use. The production of subunit vaccines in plant systems holds great promise in addressing the current challenges and facilitate the preparation for future potential outbreaks and new viruses. This review will summarize the state of development of vaccines in plant systems including tobacco, rice, maize, and others. Full article

Background: Long COVID has emerged as a global health challenge characterized by persistent neuropsychiatric symptoms, including depression, fatigue, and cognitive impairment. Growing evidence indicates that sustained neuroinflammation, endothelial dysfunction, and fronto-limbic network disruption may underlie these symptoms, representing pathophysiological features distinct from major depressive disorder (MDD). Although repetitive transcranial magnetic stimulation (rTMS) is an established treatment for MDD, its therapeutic efficacy in Long COVID-associated depression remains uncertain. Methods: Long COVID was defined as laboratory-confirmed SARS-CoV-2 infection followed by persistent neuropsychiatric symptoms lasting ≥3 months, including cognitive impairment (“brain fog”), fatigue, and new-onset depressive symptoms. We conducted a retrospective registry-based cohort study using real-world clinical data from two TMS clinics in Tokyo (May 2022–April 2026). Forty-four medication-free patients with Long COVID-associated MDD were compared with eighty-eight propensity score–matched patients with primary MDD (1:2 nearest-neighbor matching based on age, sex, and baseline Montgomery–Åsberg Depression Rating Scale (MADRS)). All participants received left dorsolateral prefrontal cortex intermittent theta burst stimulation (iTBS). Treatment outcomes were evaluated using MADRS and 17-item Hamilton Depression Rating Scale (HAM-D₁₇) improvement rates, HAM-D₁₇ response, and remission. Statistically adjusted analyses (inverse probability of treatment weighting (IPTW) and doubly robust estimation) were used to reduce measured confounding; however, residual unmeasured confounding cannot be excluded due to the retrospective observational design. Results: Long COVID patients showed significantly attenuated antidepressant response. Improvement rates were markedly lower for MADRS (38.4% vs. 61.5%) and HAM-D₁₇ (36.7% vs. 58.4%). IPTW and doubly robust models demonstrated large adjusted percentage-point differences (MADRS: −23.0 percentage points; HAM-D₁₇: −21.8 percentage points; both p < 0.001). While HAM-D₁₇ response did not differ significantly, remission rates were substantially reduced (27.3% vs. 61.4%). Conclusions: These findings indicate an adjusted association suggesting reduced rTMS responsiveness in Long COVID-associated depression. Given the retrospective observational design and the possibility of residual unmeasured confounding, the results should be interpreted as associations rather than evidence of a causal effect. Full article

Background/Objectives: Atrial fibrillation (AF) and heart failure (HF) frequently coexist, but later-pandemic data from Eastern Europe are limited. We evaluated their documented coexistence in patients hospitalized with COVID-19; the study was not designed to determine whether SARS-CoV-2 modifies the established AF–HF relationship. Methods: We retrospectively analysed 395 adults admitted with RT-PCR-confirmed SARS-CoV-2 infection between 1 September 2022 and 31 December 2024. AF was identified from the admission record, while HF was determined by an audited, rule-based review of cardiovascular free-text entries. A modified Poisson model with robust variance was the primary analysis and estimated adjusted prevalence ratios (aPRs) after adjustment for age, sex, body mass index, hypertension, ischaemic heart disease, pre-existing type 2 diabetes, chronic kidney disease, chronic obstructive pulmonary disease, smoking, and prior ischaemic stroke. Logistic regression and a restrictive NYHA-coded HF definition were sensitivity analyses. Results: AF was documented in 68 patients (17.2%), HF in 106 (26.8%), and both conditions in 26 (6.6%). HF prevalence was 38.2% among patients with AF and 24.5% among those without AF. AF was associated with documented HF in the primary model (aPR 1.51, 95% confidence interval 1.06–2.16; p = 0.022); age was also associated with HF (aPR 1.02 per year, 95% confidence interval 1.01–1.04; p = 0.010). Results were similar with the restrictive HF definition (aPR 1.54, 95% confidence interval 1.07–2.23) and logistic regression (adjusted odds ratio 1.89, 95% confidence interval 1.06–3.37). Exploratory mortality estimates were imprecise and were not used for prognostic inference. Conclusions: AF identified a subgroup with a higher prevalence of documented HF within this hospitalized COVID-19 cohort. The findings are best interpreted as evidence of cardiovascular and multimorbidity complexity, not as proof of a COVID-specific, temporal, or causal AF–HF effect. Full article

Background/Objectives: The molecular mechanisms underlying susceptibility to severe COVID-19 remain incompletely understood. We aimed to identify the signaling pathways associated with disease severity by integrating transcriptomic data and characterizing ligand–receptor interactions involved in the host response to SARS-CoV-2 infection. Methods: We integrated publicly available bulk RNA-sequencing data from nasopharyngeal (NP) swabs (GSE152075) and single-cell RNA-sequencing data from bronchoalveolar lavage fluid samples (GSE145926). Analyses focused on secreted ligands and their cognate receptors and were performed in relation to demographic and clinical characteristics associated with susceptibility to severe COVID-19, including sex, age, and viral load. Results: Patients with characteristics associated with increased susceptibility to severe disease, including male sex, advanced age, and high viral load, exhibited transcriptional programs enriched for inflammatory and immune-response pathways. In contrast, individuals with lower susceptibility displayed reduced expression of 43 ligand genes compared with matched negative controls, suggesting distinct secretory programs associated with the host response to infection. We identified an association between the expression of lactoferrin (LTF) and its receptor, LDL receptor-related protein 11 (LRP11), and susceptibility to severe COVID-19. LRP11 was predominantly expressed in human pulmonary epithelial cells, and its expression increased during SARS-CoV-2 infection in monkeys. Conclusions: Our findings provide insight into the molecular mechanisms associated with susceptibility to severe COVID-19 through the analysis of ligand and receptor expression in nasopharyngeal swabs and bronchoalveolar lavage fluid samples. The association between LTF and LRP11 highlights a potentially relevant signaling axis in disease pathogenesis and provides a rationale for future functional studies aimed at clarifying its role in COVID-19 severity. Full article

Severe coronavirus disease 2019 (COVID-19) is characterized by acute immune dysregulation, with monocytes playing a central role in driving inflammation and disease severity. However, the transcriptional and post-transcriptional regulatory mechanisms underlying monocyte dysfunction in severe COVID-19 remain unexplored. In the study, an integrative analysis of paired bulk RNA-seq and miRNA-seq datasets was performed together with independent single-cell RNA-seq (scRNA-seq) data from convalescent individuals with a history of ICU or non-ICU COVID-19. Pooled cell proportions descriptively indicated a higher proportion of classical monocytes and lower proportions of non-classical monocytes, B cells and dendritic cells in individuals with a history of ICU disease; however, none of these differences was statistically significant in patient-level analyses after multiple-testing correction. Using the miRSCAPE framework, miRNA expression was inferred at single-cell resolution and identified distinct cluster-specific inferred miRNA expression patterns. Differential expression analysis of classical monocyte populations identified 284 nominally significant differentially expressed genes between convalescent ICU and non-ICU samples. Integration of miRNA-mRNA correlation analysis with experimentally validated interactions and independent assessment highlighted a focused regulatory network centered on ZMAT3, RHOB and HLA-DQA1. Host–pathogen interaction analysis identified database-supported SARS-CoV-2-host interactions involving ORF3a-RHOB and nucleoprotein-RHPN2, with additional host–host interactions connecting RHPN2, HLA-C and HLA-DQA1. Collectively, these findings provide a computational framework for investigating inferred miRNA associations of monocyte inflammatory pathways associated with prior COVID-19 severity and highlight regulatory interactions that warrant further experimental validation. Full article

Neurologic manifestations of long COVID, also called neurologic post-acute sequelae of SARS-CoV-2 infection (Neuro-PASC: NP) include persistent alteration of cognitive functions. We investigated whether these could be driven by immune perturbations. We combined flow cytometry (FC), sleep profiling, and single-cell RNA sequencing of peripheral blood immune cells from older adult (>55 years) individuals with and without NP to evaluate relationships with objective cognitive performance. NP participants showed reduced numbers of blood monocytes with increased mitochondrial superoxide, indicating an altered monocyte mitochondrial redox state. Higher peripheral capillary oxygen saturation (SpO₂) was associated with better processing speed in NP participants. Monocyte transcriptional analyses identified mitochondrial adenosine triphosphate (ATP) synthase/Complex V (Complex V) pathway associated with cognitive performance in people without NP; this coupling was abrogated in NP patients, in whom cognitive performance instead showed an opposite relationship with Complex V. Shared leading-edge genes defined a 13-gene monocyte anchor representing this cognition-associated NP phenotype. Higher anchor scores were associated with coordinated oxidative phosphorylation and cytotoxic programs across CD3⁺ T-cell subsets in individuals without NP, but not in NP participants. T-cell receptor stratified analyses showed that this altered relationship occurred in both expanded and unexpanded T-cell populations. FC correlations also supported reduced monocyte-to-lymphocyte mitochondrial coordination in NP. These exploratory findings identify a sleep and cognition-linked monocyte mitochondrial phenotype characterized by altered myeloid–lymphoid immune coordination in NP. Full article

Objectives: The present study evaluated the association between plasma concentrations of selected endocrine-disrupting chemicals (EDCs)—bisphenol A (BPA), methylparaben (MeP), propylparaben (PrP), 4-nonylphenol (4-NP), 4-octylphenol (4-OP), bis(2-ethylhexyl) phthalate (DEHP), and imazalil (IMZ)—and prior coronavirus disease 2019 (COVID-19) status. Methods: Plasma EDC levels were quantified via gas chromatography–mass spectrometry in 262 voluntary blood donors (121 convalescents and 141 controls) at the Regional Centre for Transfusion Medicine in Bialystok, Poland. Results: The cohort exhibited widespread environmental exposure to all selected EDCs (BPA: 1.14 ng/mL, MeP: 1.20 ng/mL, PrP: 1.38 ng/mL, 4-NP: 1.90 ng/mL, 4-OP: 0.57 ng/mL, DEHP: 49.68 ng/mL, IMZ: 20.06 ng/mL). Convalescents had significantly higher concentrations of MeP, PrP, 4-OP, and 4-NP. Logistic regression revealed that MeP, PrP, and 4-NP were significantly associated with prior COVID-19 status, increasing infection odds by 80%, 70%, and 63%, respectively. While 4-OP was strongly associated with prior COVID-19 status (odds ratio > 300 per unit change and 1.79 per 0.1 unit change), the wide confidence interval for the unit change estimate requires cautious interpretation. Conclusions: These findings suggest a strong link between selected paraben and alkylphenol exposure and prior COVID-19 status in blood donors. Additionally, the high IMZ levels highlight the need for urgent evaluation of its safety and environmental prevalence. Full article

Backgroundand Objectives: Retinal microcirculation may serve as a surrogate marker of systemic vascular status and can be non-invasively assessed using optical coherence tomography angiography (OCTA). Emerging evidence suggests that retinal and choroidal microvascular alterations may occur following coronavirus disease 2019 (COVID-19) and multisystem inflammatory syndrome in children (MIS-C), potentially reflecting systemic vascular and inflammatory processes. This review summarizes the current evidence regarding retinal and choroidal microvascular changes detected by OCTA in pediatric patients with COVID-19 and MIS-C. Materials and Methods: A structured literature search of the National Center for Biotechnology Information (NCBI) PubMed database was conducted from inception until April 2026. Original English-language studies evaluating retinal and choroidal microcirculation using OCTA in pediatric patients with COVID-19 or MIS-C were identified and reviewed. Results: Available studies suggest variable retinal and choroidal microvascular alterations following COVID-19 and MIS-C, including changes in vessel density, perfusion, and foveal avascular zone parameters. Several investigations reported reduced vessel density, particularly within the deep capillary plexus, whereas others demonstrated increased peripapillary vascular parameters or no significant differences during the observation period. Differences in patient characteristics, disease severity, timing of imaging, OCTA protocols, and study design likely contribute to the heterogeneity of the reported findings. Conclusions: OCTA represents a promising research tool for investigating retinal and choroidal microvascular alterations associated with pediatric COVID-19 and MIS-C. However, the available evidence remains limited by small observational studies, methodological heterogeneity and inconsistent findings. Larger prospective longitudinal studies using standardized imaging protocols are needed to determine the clinical significance and reproducibility of OCTA-derived parameters and to establish whether they may have potential as biomarkers of ocular or systemic vascular involvement. Full article

Background: Multisystem inflammatory syndrome in children (MIS-C) was recognized in 2020 as a post-infectious hyperinflammatory condition occurring 2–6 weeks after SARS-CoV-2 infection. While large studies from Europe and North America have described its clinical spectrum and outcomes, evidence from the Middle East remains limited. MIS-C shares features with Kawasaki disease (KD), including persistent fever, mucocutaneous manifestations, and cardiac involvement, but differs in age distribution, gastrointestinal involvement, and patterns of cardiac injury. Objective: To map the reported Middle Eastern evidence on the clinical and laboratory phenotype, Kawasaki-like manifestations, cardiovascular involvement, management, short-term outcomes, and evidence gaps in children with MIS-C. Methods: A scoping review was conducted using the Arksey and O’Malley framework, guided by Joanna Briggs Institute methodology and reported according to PRISMA-ScR. PubMed/MEDLINE, Scopus, Web of Science, and the WHO COVID-19 database were searched for studies published from 1 December 2020 through 30 September 2025. Two reviewers independently screened records in Rayyan and charted data using standardized forms. Findings were synthesized descriptively; numerical ranges reflect values reported across selected contributing studies and are not pooled regional estimates. Results: Twenty-seven original clinical studies met the eligibility criteria, including case reports, case series, and observational cohorts from the UAE, Saudi Arabia, Qatar, Jordan, and multinational Middle Eastern collaborations. Across the included reports, affected children were generally older than the typical classic Kawasaki disease population. Gastrointestinal symptoms were commonly reported, and myocardial dysfunction was reported more frequently than coronary artery abnormalities. Most patients received intravenous immunoglobulin, often combined with corticosteroids. Short-term outcomes were generally favorable, but the evidence was heterogeneous and follow-up was limited. No meta-analysis was performed. Conclusions: The available Middle Eastern literature suggests that MIS-C commonly presents in school-aged children with gastrointestinal, mucocutaneous, and myocardial involvement. These patterns are descriptive rather than definitive because the evidence is predominantly retrospective, geographically uneven, and methodologically heterogeneous. The principal contribution of this review is to map the regional literature and identify priorities for prospective, standardized, multicenter studies and long-term follow-up. Full article