Search Results (10,814)

Background: Gastrointestinal (GI) involvement is increasingly recognised in paediatric SARS-CoV-2 infection and multisystem inflammatory syndrome in children (MIS-C), but severe GI bleeding remains rare. Its pathogenesis in this setting is multifactorial: direct viral injury, hyperinflammatory microvascular damage, treatment-related mucosal injury, and coagulopathy may all contribute, and the relative role of each is often difficult to disentangle. Case Presentation: A previously healthy 12-year-old boy underwent appendectomy for perforated appendicitis with peritonitis. On postoperative Day 1, he developed high fever and was found to be SARS-CoV-2 PCR-positive; SARS-CoV-2 IgM and IgG were also positive. He met the positive clinical elements of the CDC 2023 case definition for MIS-C (persistent fever, multisystem involvement—gastrointestinal, hepatic, haematological, and markedly elevated inflammatory markers), although perforated appendicitis with peritonitis is a sufficient alternative explanation and the diagnosis cannot be regarded as secure (see Discussion). Treatment included broad-spectrum antibiotics (meropenem, amikacin, metronidazole), methylprednisolone 2 mg/kg/day, and intravenous immunoglobulin (IVIG) 2 g/kg. On Day 4 in the paediatric intensive care unit (PICU), the patient developed sudden haematemesis with fresh blood through the nasogastric tube and haemodynamic collapse. Coagulation studies revealed prolonged INR (1.6) and reduced prothrombin activity (42%). The patient was stabilised with packed red blood cells, fresh frozen plasma, and intravenous vitamin K. Fibrogastroscopy demonstrated diffuse mucosal bleeding without ulcers or anatomical defects; histology showed mucosal hyperaemia, mixed basal inflammation with intraepithelial lymphocytes, and small erosions. Melena persisted for several days. The child recovered fully and was discharged after 20 days with substantially improved but not fully normalised laboratory values (residual mild anaemia, Hb 110 g/L, and elevated CRP 32.7 mg/L and D-dimer 5.88 mg/L). Conclusions: Severe upper GI bleeding is a rare but life-threatening event in children with severe SARS-CoV-2 infection and MIS-C. In our case, several mechanisms may have acted in combination, although none could be confirmed individually: possible direct viral enterocyte injury via ACE-2 receptors, hyperinflammatory microangiopathy, high-dose corticosteroid-related mucosal injury, possible broad-spectrum antibiotic-associated vitamin K deficiency, and postoperative critical-illness stress. Their relative contributions cannot be determined from a single retrospective case. Bleeding occurred despite continuous PPI prophylaxis, suggesting that PPI cover alone is insufficient when multiple risk factors coexist; the clinical implication is that risk-factor-based (rather than universal) PPI prophylaxis, together with monitoring of vitamin K-dependent coagulation, should be considered in critically ill children receiving high-dose corticosteroids and prolonged broad-spectrum antibiotics. 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

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

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

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

Background/Objective: Persistent infection with human papillomavirus type 16 (HPV-16) is the principal cause of cervical high-grade squamous intraepithelial lesions (cHSIL) and cervical cancer, yet the established treatments remain limited to ablative or excisional procedures that carry reproductive risk and do not eliminate the underlying infection. We report the preclinical development of ARV-2001, a messenger RNA (mRNA)–lipid nanoparticle (LNP) immunotherapeutic encoding mutated, non-oncogenic HPV-16 E6 and E7 fused to a SARS-CoV-2 spike S2 subdomain enriched in human CD4 helper epitopes, formulated in a novel cholesterol-derived ionizable lipid (ARV-T1). Methods: Interactions of ARV-2001-expressed antigens with p53 and retinoblastoma (Rb) were evaluated in human cervical carcinoma cell line C33A, in lentiviral constructs in primary human keratinocytes, and in soft-agar colony-formation assays. ARV-2001 was administrated by intramuscular (IM) or intradermal (ID) injection in naive mice or in the TC-1 tumor models. Tumor size and survival were monitored over time and tumor-infiltrated lymphocytes were characterized by flow cytometry. Intracellular cytokine staining and Elispot were used to evaluate immunogenicity. Results: In vitro, the mutated E6/E7–S2 antigen lost the ability to degrade p53, to deregulate the retinoblastoma (Rb) pathway, and to support anchorage-independent growth, suggesting abrogation of oncogenic activity. The S2 domain and imiquimod administration each augmented antitumor activity and intratumoral CD8⁺ T-cell infiltration while reducing myeloid-derived suppressor cells in the syngeneic HPV-16 E6/E7 TC-1 tumor models. In addition, ID administration of ARV-2001 into TC-1 tumor-bearing mice was superior to IM administration in terms of both tumor growth inhibition and survival. ID vaccination with ARV-2001 in mice consistently elicited a more potent E6/E7-specific T-cell response than the same dose given IM. Dose-escalation studies showed a dose-dependent T cell response against E6/E7 in ID-injected mice. Conclusions: This study supports future human evaluation of intradermally administrated ARV-2001 for treatment of HPV-16+ cHSIL in clinical trials. Full article

Maraviroc (MVC), a CCR5 antagonist, has been proposed as a potential antiviral agent against SARS-CoV-2; however, its mechanism of action across viral variants remains unclear. Here, we evaluated the antiviral activity of MVC against SARS-CoV-2 wild-type (WT) and Omicron BA.1 variants using single-round infectious particles (SRIPs), virus-like particles (VLPs), and cell-based assays, with a focus on its impact on viral entry and Mpro function. MVC potently inhibited infection of both WT and BA.1 SRIPs in Vero E6 cells, exhibiting EC₅₀ values of 0.0065 μM and 0.016 μM, respectively. Time-of-addition assays revealed that MVC primarily targets the early phase of infection, with the strongest inhibition observed at the viral entry stage, while moderate effects were detected during attachment and post-entry stages. Fluorescence-labeled VLP imaging demonstrated distinct entry pathways, with WT predominantly entering via plasma membrane fusion and BA.1 via endocytosis, independent of cell type. MVC altered WT-VLP trafficking by promoting internalization and lysosomal localization, whereas it had minimal impact on BA.1 internalization. In spike-mediated cell–cell fusion assays, MVC preferentially inhibited WT spike-driven syncytium formation but showed limited effects on BA.1 or BA.4 fusion, while more effectively reducing Omicron spike-mediated binding. At the post-entry stage, MVC inhibited SARS-CoV-2 main protease (Mpro) activity, with BA.1 Mpro (P132H) exhibiting greater sensitivity (IC₅₀ = 0.496 µM) than WT (1.869 µM). Collectively, these findings demonstrate that MVC exerts variant-dependent antiviral effects by targeting viral entry, modulating trafficking pathways, and inhibiting Mpro activity. This study highlights MVC as a multi-stage inhibitor with differential efficacy against SARS-CoV-2 variants, providing insights into its potential therapeutic application. Full article

Background and Objectives: The pandemic caused by the SARS-CoV-2 infection has been named coronavirus disease 2019 (COVID-19) by the World Health Organization (WHO). Cancer patients may have been more adversely affected during the COVID-19 Pandemic due to their receipt of immunosuppressive treatments, higher burden of comorbidities, and greater nutritional vulnerability compared to the general population. The aim of our study is to identify potential measures by detecting changes in the nutritional statuses of patients with an oncological diagnosis who presented to our hospital during the COVID-19 pandemic, using the globally accepted NRS-2002 questionnaire. Materials and Method: Our study included 324 patients diagnosed with malignancy who applied to the outpatient clinic of Gaziantep University, Şahinbey Training and Research Hospital, Gaziantep/Türkiye, between December 2021 and January 2022 or were hospitalized in the service. Patients included in the study were evaluated in terms of clinical–demographic information and COVID-19-related characteristics using a sociodemographic data form we developed, and then the NRS-2002 questionnaire was administered. Results: Our study included 324 patients. Overall, 49.07% (159 patients) of the patients were male, and 50.93% (165 patients) were female. A total of 20.37% of our patients (66 patients) had COVID-19 disease. While those living with their families constituted 96.91% of the patients, at least one of the family members of 36.42% of the patients had COVID-19 disease. While 76.23% (247 patients) of the patients were vaccinated, 23.77% (77 patients) were not vaccinated. When NRS analyses were examined according to the type of malignancy, a statistically significant difference was found between NRS analyses according to the type of diagnosis. When NRS analyses were examined according to the stages of the diseases, it was determined that stage 4 patients were in the risk group in terms of nutrition. When NRS analyses according to age were examined, it was determined that patients over the age of 65 were in the risk group in terms of nutrition. When NRS analyses by gender were examined, it was found that male patients were in the risk group in terms of nutrition. When the NRS analyses were examined according to whether or not radiotherapy was administered, it was determined that the patients who received radiotherapy were in the risk group in terms of nutrition. Contrary to the literature, no statistically significant difference was found according to whether or not chemotherapy was administered. Conclusions: According to NRS analysis, no statistically significant differences were found in terms of nutritional status according to COVID-19 transmission and vaccination status. When NRS analyses were examined according to the delay of treatment during the pandemic period, it was found that patients who postponed treatment were in the risk group in terms of nutrition, while patients who did not postpone treatment were mostly in the follow-up group. In multivariable analyses, however, no independent relationship was identified between this parameter and NRS-2002 risk. Full article

The emergence of SARS-CoV-2 variants and antiviral resistance highlights the need for improved therapeutic strategies against COVID-19 and other coronavirus infections. By pairing direct-acting antivirals with repurposed host-modulating drugs, combination therapy approaches may enhance antiviral efficacy while mitigating inflammation. In this study, we evaluated the effects of combining Nirmatrelvir (a SARS-CoV-2 main protease inhibitor) with Ivermectin, Azithromycin or Doxycycline—using a murine hepatitis virus (MHV) infection model of RAW264.7 macrophages. Checkerboard assays demonstrated that the Nirmatrelvir–Ivermectin combination exhibited strongly synergistic antiviral activity. This combination achieved potent inhibition of live virus titer of at least 5 to 6 log₁₀ and reduction in viral RNA load of 3 log₁₀, at drug concentrations much lower than the respective monotherapies. The Nirmatrelvir–Ivermectin combination treatment affected the coronavirus replication cycle at the same time-point of 8 h as Nirmatrelvir monotherapy. Moreover, multiplex cytokine protein profiling revealed that Nirmatrelvir–Ivermectin markedly suppressed key pro-inflammatory cytokines and chemokines associated with the cytokine storm, including IL-6, TNF-α, IL-1β, and MCP-1. Conversely, the combinations of Nirmatrelvir with Azithromycin or Doxycycline exhibited only additive or mildly additive effects, with alterations in certain cytokine levels. These findings support the potential of Nirmatrelvir–Ivermectin as a promising novel combination therapy with both antiviral and anti-inflammatory benefits, warranting further in vivo validation and clinical investigation. Full article

Pelargonium graveolens L’Hér. is a widely distributed aromatic plant that has been utilized in traditional medicine for an extended period. It is currently experiencing a surge in popularity in modern phytotherapy. The ethnopharmacological uses of this species include treatment of respiratory tract infections, digestive disorders, and analgesia. The plant’s multifaceted biological activity is attributed to the presence of monoterpenes, such as citronellol and geraniol, as well as non-volatile polyphenolic fractions and organic acids. Research has demonstrated the efficacy of PGEO (P. graveolens essential oil) in mitigating inflammation, a phenomenon attributable to the suppression of NF-κB and MAPK signaling pathways, as well as the inhibition of inflammatory mediators such as histamine, prostaglandins (PGs), and nitric oxide (NO). Furthermore, a broad spectrum of antimicrobial activity has been demonstrated against pathogens such as MRSA and Mycobacterium tuberculosis, whilst myricetin derivatives have been shown to enable the effective eradication of bacterial biofilms. It is also noteworthy that the oil’s components can reduce ACE2 receptor expression, indicating their potential to inhibit SARS-CoV-2 infection. Active compounds, such as geraniol, have been shown to modulate metabolic processes through interaction with LXR and FXR nuclear receptors. In addition, these compounds have been observed to exhibit spasmolytic effects within the gastrointestinal tract by blocking calcium channels. The influence on the HPA axis and the GABAergic system provides a scientific rationale for the plant’s traditional use in reducing stress and anxiety. Nevertheless, variations in chemical composition, determined by geographical origin, and an insufficient number of rigorous clinical data hinder the full medical implementation of this plant. It is imperative that further standardization of extracts and their verification in clinical trials is undertaken. Full article

COVID-19 affects the olfactory system and the hippocampus, leading to severe olfactory and cognitive impairments. This study aimed to quantify volumetric changes in the olfactory bulbs and hippocampus in patients with COVID-19, and to investigate these differences in relation to loss of smell and taste. This stereological MRI study included 60 COVID-19 (+) participants and 54 non-COVID-19 participants. Using OsiriX software, the volumes of the olfactory bulb and hippocampus were manually measured from 3T MRI images. Compared with controls, participants with loss of smell and taste had smaller olfactory bulb volumes. This decrease was especially noticeable in the left olfactory bulb of female patients. Furthermore, the right hippocampal volume in male patients with loss of smell and taste was significantly decreased. These findings suggest that atrophy of the olfactory bulb and hippocampus may be specific to certain regions and sexes following SARS-CoV-2 infection. Stereological MRI assessments can effectively identify these changes. Prospective longitudinal studies are needed to determine the clinical significance of these changes and their impact on patient management. Full article

Background/Objectives: Host genetic variation contributes to the heterogeneous clinical outcomes of coronavirus disease 2019 (COVID-19), yet evidence from Southeast Asian populations remains limited. Methods: We investigated host genetic factors associated with COVID-19 severity in Vietnamese patients infected with the SARS-CoV-2 Delta variant using whole-exome sequencing. A total of 48 unvaccinated patients were enrolled. During sample-level quality control, one sample was excluded because the genetically inferred sex was discordant with the information recorded in the clinical medical record, leaving 47 samples (23 severe/critical and 24 mild/asymptomatic) for downstream genetic analyses. Gene-based association analysis was performed using MAGMA, followed by functional enrichment and interaction network analyses with Metascape and GeneMANIA. Results: Population structure analysis showed that the study participants clustered closely with the East Asian (EAS) reference population. No individual variant reached the prespecified multiple-testing-adjusted threshold, and no gene-level association survived Benjamini–Hochberg correction. Using a nominal MAGMA gene-based p < 0.01 threshold solely for exploratory prioritization, 44 genes were selected for downstream functional analyses. Functional enrichment highlighted RNA processing and mRNA maturation, together with mitochondrial, metabolic, immune-regulatory, and cellular homeostasis pathways. Network topology analysis further identified several highly connected genes, including CPSF4, MRPS34, ATP5MF, BUD31, SNRPD3, and HDAC1. Conclusions: These hypothesis-generating findings are consistent with a potentially polygenic contribution to severe COVID-19 and provide an exploratory systems-level framework for understanding host genetic susceptibility in the Vietnamese population, while identifying biologically plausible candidate genes and pathways for future validation. Full article