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Seroprevalence surveys constitute a critical tool for estimating population exposure to infectious agents, particularly during public health emergencies. In the context of the coronavirus disease 2019 (COVID-19) pandemic, such surveys revealed that the circulation of Severe Acute Respiratory Syndrome Coronavirus 2 in Africa had been largely underestimated. The validity of these surveys, however, depends not only on the reliability of diagnostic tests but also on operational conditions, which are frequently challenged by fear, misinformation, and logistical constraints. In the Democratic Republic of the Congo, the National Institute of Biomedical Research conducted two seroprevalence surveys in Kinshasa in 2020 on behalf the project “Appui à la Riposte Africaine à l’Epidémie de COVID-19” (ARIACOV). This study described the challenges encountered and the adaptive strategies employed during these surveys, in order to improve future investigations. The study population comprised 41 eligible field workers who participated in the 2020 ARIACOV seroprevalence surveys in Kinshasa, including 28 interviewers and 13 specimen collectors. Of these, 24 individuals (16 interviewers and 8 specimen collectors) initially confirmed their participation. Ultimately, 15 participants took part in the focus group discussions, comprising 11 interviewers (39.3% of the 28 eligible interviewers) and 4 specimen collectors (30.8% of the 13 eligible specimen collectors). We collected data through two focus groups held in a single session, using a pre-tested semi-structured guide. Discussions were audio-recorded and complemented by observational notes until empirical saturation was achieved. We applied deductive thematic analysis, following Braun and Clarke’s framework, to three predefined domains: transportation, survey procedures, and sample management. The application of systematic manual coding, combined with researcher triangulation, reinforced the rigor and enhanced the credibility of the findings. The findings highlighted community mistrust, driven by rumors, apprehension regarding blood collection, financial suspicions, and inadequate communication. In addition, logistical and transportation challenges significantly constrained survey feasibility. Nonetheless, a range of adaptive strategies were implemented, enabling the successful conduct of the surveys despite the pandemic context and limited resources. The participants’ narratives suggest that strengthening field workers’ training, improving transparency, and working alongside community health workers could contribute to enhance the effectiveness of serological surveys during health crises in resource-constrained environments. Full article

Background: Coronavirus disease 2019 (COVID-19) has been associated with thyroid dysfunction; however, evidence from primary care settings remains limited. Given that most patients with COVID-19 are managed outside hospital settings, understanding thyroid function changes in real-world primary care is clinically relevant. Methods: This retrospective study included 373 adult outpatients with confirmed COVID-19 and no prior thyroid disease, who were managed in a Family Medicine Clinic in Warsaw between January of 2022 and December of 2024. Thyroid function tests (yielding TSH, fT3, and fT4 levels) obtained within three months before and after infection were analyzed. Subacute thyroiditis (SAT) was assessed in symptomatic patients via thyroid ultrasound. Paired comparisons were performed, with p < 0.05 considered statistically significant. Results: A significant reduction in the mean TSH level was observed following COVID-19 compared with pre-infection values (mean 2.39 vs. 2.17 mIU/L; p < 0.05), while fT3 (2.93 vs. 2.98 pg/mL) and fT4 (1.31 vs. 1.30 ng/dL) concentrations remained unchanged. No significant associations were found between thyroid function changes and age or sex. Conclusions: In this real-world primary care population, lower TSH concentrations were observed following COVID-19 while peripheral thyroid hormone levels remained unchanged, suggesting predominantly modest changes in thyroid function parameters. Given the retrospective study design and the absence of a control group, these findings should be interpreted with caution. Further prospective studies are needed to clarify the clinical significance of post-COVID-19 thyroid function changes. Full article

Coronavirus disease 2019 (COVID-19) causes systemic inflammation and multi-organ injury that may persist beyond the acute illness. The Fibrosis-4 (FIB-4) index and the aspartate aminotransferase-to-platelet ratio index (APRI) are inexpensive liver fibrosis scores whose long-term prognostic value after COVID-19 pneumonia is undefined. In this single-center retrospective study, 101 adults hospitalized with severe COVID-19 pneumonia were followed for three years. FIB-4, APRI, and the chest computed tomography (CT) severity score were derived from admission data. Discrimination was quantified by the area under the receiver operating characteristic curve (AUC) and compared with the DeLong test; nested logistic regression models tested whether FIB-4 added prognostic information beyond age. Fifty-seven patients (56.4%) died, 39 in hospital and 18 after discharge. Admission FIB-4 was higher in non-survivors (median 3.0 vs. 1.5; p < 0.001), whereas APRI did not differ. FIB-4 showed superior prognostic accuracy for mortality compared to APRI (AUC 0.746 vs. 0.595; p = 0.002) and CT severity score (AUC 0.490; p = 0.001), while performing comparably to age alone (AUC 0.756; p = 0.870). Log-FIB-4 remained associated with mortality after adjustment for age (odds ratio 2.04, 95% CI 1.10–3.76) but not after further adjustment for C-reactive protein and creatinine (odds ratio 1.75, 0.86–3.55), whereas FIB-4 > 2.44 retained an age-adjusted odds ratio of 5.90 (2.20–15.83). Among patients discharged alive, FIB-4 was not associated with subsequent death. Admission FIB-4 was independently associated with three-year mortality and outperformed APRI and the CT severity score, but its prognostic information largely overlapped with age; it should be regarded as a composite admission risk index whose added value requires external validation. Full article

Coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), exposed critical gaps in global preparedness for rapidly evolving viral pandemics. Though current antiviral treatments have shown some efficacy in managing COVID-19, substantial limitations, such as inefficient targeted drug delivery, aberrant host immune responses, and inadequate preparedness for future viral pandemics, were also evident. These challenges underscore the urgent need for target-specific, precise and efficient therapeutic strategies to modulate viral entry and immune dysregulation. Extracellular vesicles (EVs), cell-released cargo-carrying nanoscale vesicles, can both facilitate and inhibit viral infection depending on their cargo composition. Thus, endogenous EVs can promote or inhibit COVID-19 pathogenesis by modulating critical pathways, including angiotensin-converting enzyme 2 (ACE2)-mediated viral entry, transmembrane protease serine 2 (TMPRSS2)- dependent spike protein activation, nuclear factor kappa B (NF-κB)-driven inflammatory signaling, and NLRP3 inflammasome activation. In contrast, engineered EVs, such as ACE2-expressing EVs, mesenchymal stem cell-derived EVs and microRNA-enriched EVs, have therapeutic potential as they can facilitate antiviral defense through immune modulation, viral neutralization and suppression of cytokine storm. Moreover, EV-associated nucleic acids, proteins and lipids can act as biomarkers for disease detection and severity stratification. A deeper understanding of EV-virus mechanistic insights can enhance preparedness for similar viral diseases. In this review, we provide a comprehensive analysis of the molecular mechanisms underlying EV-virus interactions highlighting the therapeutic and diagnostic potential of EVs in tackling COVID-19 and future viral pandemics. Full article

Background/Objectives: Host factors angiotensin-converting enzyme 2 (ACE2), transmembrane protease-serine 2 (TMPRSS2), furin paired basic amino acid cleaving enzyme (FURIN), and neuropilin-1 (NRP1) facilitate severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) entry, but it is unclear whether their upper-airway expression after recovery is associated with the severity of the preceding acute illness. We examined the association between post-acute expression of these genes and previous coronavirus disease 2019 (COVID-19) severity. Methods: This multicenter cross-sectional study included 104 adults with polymerase chain reaction (PCR)-confirmed COVID-19 during the first two pandemic waves in Murcia, Spain. Nasal and/or oropharyngeal swabs were collected in the post-acute phase, at a median of 75 days after symptom onset, and transcript levels were quantified by quantitative real-time PCR. Severity was categorized using the World Health Organization (WHO) Clinical Progression Scale, and associations were evaluated using logistic regression adjusted for age, sex, and race/ethnicity. Results: In the primary analyses using continuous expression measures, none of the four genes was significantly associated with severity. In exploratory tertile-based analyses, the intermediate ACE2 tertile (odds ratio [OR] = 0.17, 95% confidence interval [CI] 0.05–0.61; p = 0.007) and intermediate NRP1 tertile (OR = 0.29, 95% CI 0.10–0.88; p = 0.030) were associated with lower odds of severe disease; no significant associations were observed for the high tertiles or for FURIN or TMPRSS2. Conclusions: Primary adjusted analyses did not reveal statistically significant associations between post-acute nasal expression of ACE2, TMPRSS2, FURIN, or NRP1 and COVID-19 severity. Because expression was measured after clinical recovery, these associations cannot be interpreted as predictors of acute severity and may instead reflect persistent molecular remodeling after more severe disease; reverse causation cannot be excluded. Longitudinal studies with acute-phase and serial post-acute sampling and healthy controls are needed. Full article

From a health perspective, the 21st century has witnessed the emergence and global impact of several major viral diseases, most notably coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2, which has been associated with a substantial burden of secondary fungal infections. Patients suffering from COVID-19 illnesses frequently developed fungal co-infections, which can worsen clinical outcomes and complicate therapeutic efforts. Hospitalized individuals with viral infections are particularly susceptible to invasive fungal pathogens, including Aspergillus, Candida, and Mucorales species. The co-pathogenesis between respiratory virus and fungi is complex, involving dynamic interactions among the pathogens and the host immune system. Opportunistic fungal infections were found to be more prevalent in COVID-19-infected individuals, who require mechanical ventilation, have diabetes, or exhibit neutropenia. This review aims to provide a comprehensive overview of fungal co-infections associated with COVID-19 disease, with a focus on their pathogenesis, biomarkers, diagnostic approaches, and potential treatment strategies. Overall, the available evidence indicates that viral-induced immune dysregulation, epithelial barrier damage, and clinical risk factors contribute to the development and severity of fungal co-infections in COVID-19 patients. Early recognition using reliable biomarkers and standardized diagnostic approaches, together with timely and pathogen-directed antifungal therapy, are essential for improving clinical outcomes. Full article

Background: During the coronavirus disease 2019 (COVID-19) pandemic, changes in healthcare organisation may have affected the management of patients with chronic conditions, such as those with type 2 diabetes (T2D), who require close monitoring. Although there are studies that have analysed the access and management of patients with T2D in primary care (PC) during the pandemic, there is no synthesis of the results that inform us about the care provided and their effect. The aim of this study is to summarise the existing evidence on the care provided in PC settings to patients with T2D during the COVID-19 pandemic, as well as their follow-up care and outcomes, in order to understand the impact of the pandemic on their management. Methods: A scoping review was conducted according to the approach described by Arksey and O’Malley. Structured search strategies were developed for each of the selected databases (PubMed, EMBASE and Web of Science). We included articles published in English and Spanish up to 24 March 2026 on access to care for patients with T2D in PC during the pandemic. Two independent reviewers screened titles and abstracts to select studies related to the population, intervention, and outcomes of interest. In cases of disagreement, a third reviewer resolved the discrepancy. One of the reviewers extracted data and summarised them. Results: After duplicate removal, 535 records were identified, with 116 articles screened in full text and 26 included. Most studies were conducted in Europe and North America using retrospective designs and electronic health records. During the pandemic period, face-to-face visits and routine screenings generally declined, while telemedicine expanded and may have partially mitigated disruptions in patient contact, although inequalities in access were reported. Disease monitoring and complication screening also declined in several settings. Clinical outcomes such as HbA1c and blood pressure (BP) showed heterogeneous trends, with some studies reporting deterioration and others reporting stability. Some studies also highlighted increased adverse events and greater attention to mental health during care. Conclusions: Although telemedicine helped maintain patient follow-up, it could not fully replace face-to-face assessments and was implemented alongside some gaps in clinical monitoring, patient safety, and health equity. These findings underscore the need to maintain structured chronic disease management and to develop safe and inclusive telehealth models. Full article

Platelet activation plays a central role in arterial thrombosis, thromboinflammation, and microvascular injury. Conventional platelet function tests evaluate platelet responsiveness to exogenous agonists ex vivo but do not directly reflect in vivo platelet activation. Although several soluble platelet-derived molecules, including platelet factor 4 (PF4), β-thromboglobulin (β-TG), soluble P-selectin, soluble CD40 ligand, glycocalicin, and soluble glycoprotein (GP) VI, have been investigated as in vivo platelet activation markers, their clinical use is limited by preanalytical instability, lack of platelet specificity, constitutive shedding, or uncertain disease specificity. Soluble C-type lectin-like receptor 2 (sCLEC-2) has recently emerged as a promising biomarker of in vivo platelet activation. CLEC-2 is expressed predominantly in platelets and megakaryocytes, and its soluble form is released from activated platelets as both a shed molecule and a microparticle-associated form. Compared with PF4 and β-TG, sCLEC-2 is less susceptible to artifactual release during routine blood collection, making it more suitable for clinical laboratory testing. Elevated sCLEC-2 levels have been reported in acute coronary syndrome, acute ischemic stroke, disseminated intravascular coagulation, thrombotic microangiopathy, antiphospholipid antibody syndrome, and coronavirus disease 2019 (COVID-19). In thrombocytopenic disorders, indices incorporating platelet count, such as the C2PAC index, sCLEC-2/D-dimer ratio, and sCLEC-2 × D-dimer/platelet count, may better reflect platelet activation and disease status than sCLEC-2 concentration alone. However, preanalytical standardization, assay harmonization, reference interval validation, and disease-specific cutoff values remain essential. This review summarizes the biological basis, assay systems, clinical evidence, and future perspectives of sCLEC-2 as an emerging laboratory marker of in vivo platelet activation. Full article

Background: Preoperative anaemia and perioperative transfusion are associated with adverse outcomes after cardiac surgery with cardiopulmonary bypass (CPB). Coronavirus disease 2019 (COVID-19) may induce persistent haematological and endothelial alterations. Whether previous infection modifies the relationship between haemoglobin and outcomes is unclear. This study evaluated whether previous COVID-19 infection modified the association between preoperative haemoglobin concentration and perioperative transfusion burden after cardiac surgery with CPB. Early postoperative complications were analysed as predefined secondary outcomes. Methods: This study represents a secondary analysis of a prospective observational cohort of adult patients undergoing elective on-pump cardiac surgery between 1 August 2022 and 30 October 2023. Patients were categorised according to previous COVID-19 infection. Surgery was performed at least seven weeks after infection. The primary outcome was perioperative transfusion burden, defined as the total number of blood products administered from the intraoperative period until hospital discharge. An interaction term between previous COVID-19 and preoperative haemoglobin was included in multivariable linear regression. Results: A total of 280 patients were included, of whom 101 (36.1%) had a previous COVID-19 infection. Preoperative haemoglobin was comparable between patients with and without a previous COVID-19 infection (13.4 [12.4–14.8] vs. 13.8 [12.2–14.6] g/dL; p = 0.472). No significant differences in early postoperative complications, transfusion rates, or transfusion burden were observed according to previous COVID-19 infection. The COVID-19 × haemoglobin interaction was not statistically significant in the adjusted model (B = 0.002, 95% CI −0.081 to 0.085; p = 0.958). Lower preoperative haemoglobin, lower baseline platelet count, longer CPB duration, and CKD were independently associated with greater transfusion burden. In an exploratory multivariable analysis, preoperative anaemia remained associated with postoperative AKI after adjustment for relevant covariates (adjusted OR 5.80, 95% CI 2.23–15.06; p < 0.001). Conclusions: No statistically significant interaction between previous COVID-19 and preoperative haemoglobin was demonstrated for perioperative transfusion burden. Lower preoperative haemoglobin was independently associated with greater transfusion burden, while preoperative anaemia remained associated with postoperative AKI after multivariable adjustment in an exploratory analysis. These findings support systematic preoperative anaemia screening and Patient Blood Management in cardiac surgery. 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

Background/Objectives: Mechanical power (MP) quantifies the energy delivered to the respiratory system during ventilation and serves as a promising marker for ventilator-induced lung injury (VILI). According to its original definition by Gattinoni, MP reflects the energy transferred from the ventilator to the respiratory system under conditions of deep sedation, passive breathing, neuromuscular blockade, and volume-controlled ventilation. Its role in coronavirus disease 2019 (COVID-19)-associated acute respiratory distress syndrome (ARDS) remains under investigation. This systematic review aimed to synthesize the available evidence on the association between MP and VILI, complications related to mechanical ventilation (MV), and mortality in adult patients with COVID-19 undergoing invasive mechanical ventilation (IMV). Methods: A systematic review was conducted using PubMed-MEDLINE (Medical Literature Analysis and Retrieval System Online) for studies published in recent years, focusing on adult COVID-19 patients undergoing IMV. Inclusion criteria centered on studies reporting MP and its association with VILI, complications, or mortality. Ten studies met eligibility criteria after screening 356 retrieved articles. Results: Most included studies were retrospective and observational, encompassing critically ill COVID-19 patients. Elevated MP was correlated with more severe outcomes, including increased 28-day mortality, prolonged MV, and weaning failure. Franck et al. demonstrated strong correlations between MP and driving pressure, elastance, and positive end-expiratory pressure, emphasizing the importance of calculation methods. González-Castro et al. identified a threshold of 17 J/min, above which mortality risk increased. Stalla et al. highlighted that dynamic MP reductions during prone positioning were associated with survival. Registry-based analyses confirmed that both magnitude and cumulative exposure above 18 J/min increased intensive care unit mortality. Novel indices combining MP with oxygenation parameters improved prognostic accuracy. While absolute MP at initiation provided limited predictive value, temporal trends and individual components were strongly linked to VILI. Conclusions: Higher MP has been associated with adverse clinical outcomes in patients with COVID-19 receiving invasive mechanical ventilation, supporting its potential role as a prognostic indicator. Its dynamic assessment, thresholds, and integration with ventilatory strategies such as prone positioning enhance risk stratification and may guide individualized, lung-protective ventilation. Continuous monitoring and standardized calculation are recommended to optimize clinical decision-making. 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

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