Background: Chronic low-grade inflammation and dyslipidemia contribute to metabolic disorders such as diabetes. Dysglycemia, an early stage of glucose dysregulation, reflects this interplay. The neutrophil-to-HDL cholesterol ratio (NHR) integrates inflammatory and lipid pathways, but its role in dysglycemia, particularly in Middle Eastern populations, remains unclear. This study evaluated the association between NHR and glycemic abnormalities, including impaired fasting glucose (IFG) and hyperglycemia (HG). Methods: A retrospective cross-sectional investigation involving 13,121 individuals at a major health setting in Saudi Arabia was conducted. The association between NHR and glycemic status was comprehensively evaluated, with subgroup analyses stratified by age and gender. Risk and diagnostic performance of NHR for dysglycemia were evaluated. Correlation and linear regression analyses were conducted to examine the relationships between NHR and fasting glucose, as well as HbA1c. Results: NHR levels were significantly associated with dysglycemia, showing progressive elevation from normoglycemia (5.30: 3.453–7.755) to IFG (6.00: 3.904–8.663) and HG (7.177: 4.917–10.17). Elevated NHR was more prevalent among individuals with dysglycemia and was associated with an increased risk of IFG (OR = 1.48, 95% CI: 1.36–1.61, p < 0.0001) and HG (OR = 2.38, 95% CI: 2.13–2.65, p < 0.0001). In the FBG context, NHR showed better discrimination of HG from NG than CRP (AUC = 0.650 vs. 0.570; p < 0.0001). Conclusions: Elevated NHR is significantly associated with dysglycemia, particularly hyperglycemia. These findings suggest that NHR may serve as a supportive tool for identifying individuals at increased risk of dysglycemia, especially in populations with limited diagnostic resources. Future longitudinal studies are warranted to validate its predictive and prognostic value in clinical practice.

Seasonal human coronaviruses (HCoVs) continue to undergo adaptive evolution under structural and immune-mediated constraints. We investigated the molecular epidemiology and spike (S) protein structural variation of circulating coronaviruses in Riyadh, Saudi Arabia, during the 2025–2026 winter season, with particular emphasis on genotype persistence and glycosylation architecture in HCoV-OC43. Among 293 nasopharyngeal aspirates (NPAs) collected from hospitalized patients with acute respiratory illness, HCoV-OC43 was detected in 26 cases (8.87%), whereas other seasonal coronaviruses were not identified. Partial sequencing of the S gene revealed 97.84–98.23% nucleotide identity relative to the prototype strain VR-759, with amino acid substitutions distributed at discrete positions rather than within extended variable domains, indicating structural conservation. Phylogenetic reconstruction demonstrated that all Riyadh isolates clustered within genotype C, together with previously circulating local strains, supporting sustained endemic persistence and in situ evolution. In silico analysis of the S protein glycosylation landscape identified four invariant N-linked glycosylation motifs (N-X-S/T) at residues 46, 121, 134, and 190, reflecting strong structural constraints on glycan-dependent folding and antigenic configuration. A genotype-associated K68N substitution generated an additional N-glycosylation motif (68NGTD) in multiple Riyadh isolates, potentially modifying local glycan shielding without disrupting the overall glycosylation framework. The preservation of core glycosylation sites alongside selective motif acquisition suggests evolutionary fine-tuning of S surface topology rather than large-scale structural remodeling. Collectively, these findings indicate that genotype C persistence in Riyadh is accompanied by conserved S architecture and subtle glycosylation adjustments that may modulate immune recognition while maintaining structural integrity. Continued high-resolution molecular surveillance will be critical for defining the functional consequences of S microevolution in endemic HCoVs.

We analysed nine Pseudomonas guariconensis-clade genomes from environmental and clinical sources across four continents to test whether carriage of acquired resistance is associated with the acquisition of mobile elements. FA-1, our tick-derived anchor from Hyalomma dromedarii on Saudi camels, sits at 87.52–87.94% ANI to the other genomes on the longest external branch of the core-genome ML phylogeny. In the current NCBI type-strain ANI taxonomy check, FA-1 is conspecific with the recently described Pseudomonas shiyinii type strain ST4 (98.05% ANI). The recently reported Vietnamese hospital-wastewater isolate KNHN1 groups within the sensu stricto clinical clade alongside USA-Nashville and India at 99.7%/99% (SH-aLRT/UFBoot) support. Across the nine genomes, three distinct carbapenemase architectures emerged: Dao (chromosomal KPC-2 + NDM-1 + AFM-5), Ethiopia (chromosomal NDM-1 × 2 + plasmid VIM-4), and Korea (plasmid VIM-2). Dao and Ethiopia chromosomes share a MOBH-family relaxase signal, extending the MOBH marker to the clinical compartment. MBL-positive genomes carried more mobile elements (Dao 55; Ethiopia 22; Korea 16; 16–55 hits) than MBL-negative comparators (0–8 hits), an unadjusted descriptive observation (n = 3 vs. 6). Ethiopia presented an integron-rich chromosomal and plasmid architecture (six structures), while Dao carried IS-bounded transposon islands on the chromosome. Three of four Dao chromosomal ICE predictions and one Ethiopia ICE prediction lay 27–50 kb from IS-bounded carbapenemase loci; a fourth Dao ICE was standalone and the major Ethiopia NDM-1 + OXA-10 cassette lacked an adjacent complete ICE prediction, indicating descriptive ICE-cassette proximity rather than functionally demonstrated mobility. Together, these findings are consistent with mobile-element acquisition as a plausible route for the emergence of clinical resistance within this clade, with environmental relatives retaining empty insertion sites at the AMR-cassette locus.

Background and Objectives: Hepatitis B virus (HBV) infection remains a major cause of progressive liver disease worldwide. Although HBV DNA reflects viral replication, its relationships with conventional liver biochemical markers and non-invasive indices remain insufficiently studied in Saudi patients. This study evaluated the associations of HBV DNA level with conventional liver-related parameters, the Albumin–Bilirubin (ALBI) score, and the Fibrosis-4 (FIB-4) index. Materials and Methods: This retrospective cross-sectional study included patients with HBV infection evaluated at King Khalid University Hospital between January 2015 and June 2026. Laboratory data collected within 12 months of the recorded diagnosis date were used to calculate ALBI and FIB-4 scores. Relationships between HBV DNA and liver-related parameters were evaluated using Spearman correlation and group comparisons based on a predefined threshold of 2000 IU/mL. Multivariable logistic regression assessed factors associated with ALBI Grades 2–3. Results: Among 394 patients, median liver enzyme levels were generally within their reference ranges, although 55.7% of patients with available data had ALBI Grades 2–3. Among 160 patients with quantifiable HBV DNA, viral load correlated significantly with all seven evaluated liver-related parameters in the full analytical cohort, with AST showing the strongest association (ρ = 0.437, p < 0.001), although sensitivity analyses suggested these associations may partly reflect treatment-related differences in viral load distribution. Patients with HBV DNA ≥2000 IU/mL had significantly different liver-related parameters than those below this threshold. Each tenfold increase in HBV DNA was associated with 69% higher odds of ALBI Grades 2–3 (OR = 1.69; 95% CI: 1.32–2.25; p < 0.001). ALBI and FIB-4 were moderately positively correlated (ρ = 0.392, p < 0.001). Conclusions: Higher HBV DNA levels were associated with differences in liver-related parameters and poorer ALBI grade. Combining viral-load measurement with conventional markers and non-invasive indices may provide a more comprehensive assessment of hepatic involvement in HBV infection.

Background: Respiratory tract infections (RTIs) caused by viruses are a public health problem, contributing to hospital admissions and morbidity worldwide. The COVID-19 pandemic substantially altered the detection patterns of respiratory viruses through public health interventions. Longitudinal data on these changes and viral seasonality remain limited in Saudi Arabia. This eight-year study evaluated epidemiological and seasonal patterns of major respiratory viruses across the COVID-19 era at a major Saudi tertiary care center. Methods: A retrospective observational study was conducted at King Khalid University Hospital, Riyadh, from October 2017 to December 2025. PCR-confirmed detections for SARS-CoV-2, Influenza A, Influenza B, respiratory syncytial virus (RSV), and human metapneumovirus (HMPV) were extracted from the hospital Laboratory Information System. Demographics, co-detection, seasonality, and length of stay (LOS) were analyzed across four eras spanning the pre-COVID-19, lockdown, restriction, and post-restriction periods using descriptive statistics, the Kruskal–Wallis test, and multivariable negative binomial regression. Results: Among 5708 confirmed respiratory viral detection episodes, SARS-CoV-2 was the most frequently detected (52.5%), followed by Influenza A (19.1%), RSV (16.4%), Influenza B (8.4%), and HMPV (3.6%). Before the pandemic, Influenza A accounted for the largest proportion of detected episodes (71.1%), with detections clustering particularly during autumn and winter seasons, whereas SARS-CoV-2 accounted for the majority of detected episodes during the lockdown and restriction eras (97.4% and 93.2%). The post-restriction era became more diverse, with RSV being detected in substantial proportions (28.3%), showing prominent winter activity. RSV and HMPV predominantly affected children aged 0–5 years, whereas SARS-CoV-2 was more frequently detected among older adults. Among adults, older age was associated with prolonged LOS; Influenza A and HMPV were associated with shorter stays compared to SARS-CoV-2. Among children, no virus was independently associated with LOS after adjustment for age and sex; however, older age was associated with longer hospital stays. Conclusion: The observed detection patterns of major respiratory viruses shifted substantially across the COVID-19 eras, with notable post-restriction diversification among observed positive detections. LOS was associated with age in both adults and children and with virus type among adults, supporting continued surveillance to guide preventive and clinical strategies.