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Interleukins (ILs) are signaling molecules that are crucial in reguLating immune responses during infectious diseases. Pro-inflammatory ILs contribute to the activation and recruitment of immune cells, whereas anti-inflammatory ILs help to suppress excessive inflammation and promote tissue repair. Here, we provide a comprehensive overview of the role of pro-inflammatory and anti-inflammatory ILs in infectious diseases, with a focus on the mechanisms underlying their effects, their diagnostic and therapeutic potential, and emerging trends in IL-based therapies.

Malaria is still one of the major global health challenges affecting millions annually, particularly in non-Mediterranean Africa and Southeast Asia. Over the past two decades, substantial progress has been made in reducing malaria-related morbidity and mortality, primarily due to advancements in antimalarial therapeutics. This review provides a comprehensive overview of recent developments in malaria treatment, focusing on the evolution of drug therapies, mechanisms of action, and emerging resistance patterns. The cornerstone of current treatment strategies is artemisinin-based combination therapies (ACTs), which have proven highly effective against P. falciparum and P. vivax, the most prevalent malaria-causing parasites. However, the onset of artemisinin resistance, particularly in Southeast Asian countries, poses a significant threat to these gains. Additionally, other antimalarial classes, including quinine derivatives, 8-aminoquinolines, and antifolate drugs, are examined for their efficacy, resistance mechanisms, and future potential. This review also discusses the challenges associated with drug resistance, the genetic underpinnings of resistance in malaria parasites, and the implications for future treatment protocols. Furthermore, the review examines combinational therapies, such as triple artemisinin combination therapies (TACTs), and vaccines that are approved or in development to circumvent resistance issues. The need for continuous surveillance, innovative therapeutic strategies, and advances in novel antimalarial therapeutic agents is emphasized to sustain and further progress in the control of malaria and its eventual eradication.

Coronavirus disease (COVID-19) is reported as a complex disorder affecting multiple systems and coagulopathy that can cause mortality. In this study, we investigated the correlation of SARS-CoV-2 mutations found in blood samples with various changes in the fibrinolysis system, as well as the severity of the disease based on outcome and whether or not these patients were admitted into the ICU. COVID-19 patients (n = 446) admitted to our institute between 2021 and 2022 were recruited. Blood samples were collected, and a sequence analysis of the SARS-CoV-2 spike gene was isolated from the blood. Measured several parameters of fibrinolysis and coagulation, including alpha-2-antiplasmin and plasminogen, thrombin activatable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), D-dimer, and fibrinogen levels. SARS-CoV-2 RNA was found in 123/446 (27.6%) of the blood samples. The N501Y, D614G, K417N, and P681R mutations among COVID-19 patients were associated with higher admissions to the ICU (P = 0.0057, P = 0.0068, P = 0.0193, and P = 0.018, respectively). Omicron (BA.1.1) variant variants are highly associated with thrombosis (P = 0.002) in hospitalized COVID-19 patients that are unvaccinated and have comorbidity conditions. The plasma levels of tPA, aPTT, and D-dimer were significantly higher in participants who had the N501Y mutation (P = 0.044, P = 0.024, and P = 0.027, respectively). Thrombosis was the most prevalent condition among severe COVID-19 patients. The correlation between specific SARS-CoV-2 new variants and thrombosis warrants more investigation.

Background: COVID-19 is associated with coagulopathy and increased mortality. The ABO blood group system has been implicated in modulating susceptibility to SARS-CoV-2 infection and disease severity, but its relationship with viral RNAemia, spike gene mutations, and thrombosis remains underexplored. Methods: We analyzed 446 hospitalized COVID-19 patients between 2021 and 2022. SARS-CoV-2 RNAemia was assessed via RT-qPCR on whole blood, and spike gene mutations were identified through whole-genome sequencing in RNAemia-positive samples. ABO blood groups were determined by agglutination testing, and thrombotic events were evaluated using coagulation markers. Statistical analyses included chi-square tests and Kruskal–Wallis tests, with significance set at p < 0.05. Results: RNAemia was detected in 26.9% of patients, with no significant association with ABO blood group (p = 0.175). Omicron was the predominant variant, especially in blood group A (62.5%). The N501Y mutation was the most prevalent in group O (53.2%), and K417N was most prevalent in group B (36.9%), though neither reached statistical significance. Thrombotic events were significantly more common in blood group A (OR = 2.08, 95% CI = 1.3–3.4, p = 0.002), particularly among RNAemia-positive patients. Conclusions: ABO blood group phenotypes, particularly group A, may influence thrombotic risk in the context of SARS-CoV-2 RNAemia. While no direct association was found between blood group and RNAemia or spike mutations, the observed trends suggest potential host–pathogen interactions. Integrating ABO typing and RNAemia screening may enhance risk stratification and guide targeted thromboprophylaxis in COVID-19 patients.

Nanoparticles have shown promising potential for efficient drug delivery, circumventing biological interferences like immunological and renal clearance and mechanical and enzymatic destruction. However, a handful of research papers have questioned the biomedical use of metal-based nanoparticles like cadmium telluride quantum dots (CdTe-QDs) for their cytotoxic, genotoxic, and carcinogenic potential. Herein, we examined the effects of CdTe-QD NPs on gene expression profile of hepatocellular carcinoma (Huh-7) cell line. Huh-7 cells were treated with CdTe-QD NPs (10 μg/ml for 6, 12, and 24 hours, and 25 μg/ml for 6 and 12 hours), and transcriptomic analysis was performed using microarray to evaluate the global gene expression profile. Differential expressed genes (DEGs) were observed for both the doses (10 and 25 μg/ml) of CdTe-QD NPs at different time points. Gene ontology (GO) analysis revealed that genes involved in molecular function of cell cycle, organizational injury and abnormalities, cell death and survival, gene expression, cancer, organismal survival, and cellular development were differentially expressed. Overall, we have demonstrated differential expression of several genes, involved in maintaining cell survival, metabolism, and genome integrity. These findings were confirmed by RT-qPCR study for some canonical pathway genes signifying possible implication in NP toxicity-mediated cell survival and inhibition of cell death.

Abnormal transcriptomic profiles of coagulation genes have been linked to coagulopathies in patients with coronavirus disease 2019 (COVID-19). The objective of the present study was to explore the frequency of genotypes and potential association of polymorphisms in genes encoding coagulation factors with the disease severity in COVID-19 patients. The patients were clinically categorized into four groups of COVID-19 disease severity (asymptomatic, mild, moderate, and severe). Three variants of genes, involving the coagulation genes rs3136516 (F2 gene), rs6042 (F7 gene), and rs6123 (PROS1 gene), were studied. Polymorphisms were genotyped by Sanger DNA sequencing. Most of the subjects had moderate COVID-19 infection (n = 53, 62.4%), followed by mild (n = 16, 18.8%), and severe infections (n = 15, 17.6%). The frequency of the rs3136516 AG genotype was considerably higher in non-ICU patients compared to ICU patients (51.3% vs 34.1%, OR 3.167, 95% CI 1.094-9.170, P = .031). Furthermore, the dominant genetic model (AA + AG vs GG) was significantly associated with a decreased probability of admission to the ICU in COVID-19 patients (OR 0.340, 95% CI 0.127 - 0.905, and P = .028). No other variants of the coagulation genes studied were found to be associated with the severity of COVID-19 disease, admission to the ICU, and mortality (P > .05). The rs3136516 AG genotype could predispose COVID-19 patients to increased disease severity and therefore admission to the ICU, while the dominant genetic model (AA + AG vs GG) of rs3136516 exerts a protective role.

Interleukin-37 (IL-37) has recently been recognized as a strong anti-inflammatory cytokine having anti-tumor activity against hepatocellular carcinoma (HCC) in hepatitis B virus (HBV)-infected patients. HCC is a typical inflammation-related cancer, and genetic variations within the IL-37 gene may be associated with the risk of HBV infection. Identification of the allelic patterns that genetically have a high disease risk is essential for the development of preventive diagnostics for HBV-mediated liver disease pathogenesis. In this study, we aimed to investigate the association between single nucleotide polymorphisms (SNPs) within the IL-37 gene and disease sequelae associated with HBV infection. We genotyped ten IL-37 SNPs in 1274 patients infected with HBV and 599 healthy controls from a Saudi Arabian population. Among the selected SNPs, two SNPs (rs2723175 and rs2708973) were strongly associated with HBV infection, and six SNPs (rs2723176, rs2723175, rs2723186, rs364030, rs28947200, rs4392270) were associated with HBV clearance, comparing healthy controls and HBV infected-patients respectively. A suggestive association of rs4849133 was identified with active HBV surface antigen (HBsAg) carrier and HBV-related liver disease progression. In conclusion, our findings suggest that variations at the IL-37 gene may be useful as genetic predictive risk factors for HBV infection and HBV-mediated liver disease progression in the Saudi Arabian population.

Introduction: In this study, coagulation and fibrinolysis parameters and their association with disease severity were investigated in coronavirus disease (COVID-19) patients. Materials and Methods: COVID-19 patients (n = 446) admitted to our institute between 21 February 2021 and 17 March 2022, were recruited. Clinical data and staging were collected from all patients. Blood samples were collected and analyzed for several parameters of fibrinolysis and coagulation, including alpha-2-antiplasmin(α2AP) and plasminogen, thrombin activatable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), D-dimer, and fibrinogen levels. Results: The TAFI, fibrinogen, and tPA levels were significantly higher in participants who died compared to that of patients who recovered (p < 0.001). However, PAI-1, tPA, and TAFI were significantly higher in patients admitted to the ICU than those of the healthy controls (p < 0.001 for PAI-1 and tPA; p = 0.0331 for TAFI). Our results showed that stage C and D COVID-19 patients had significantly higher levels of PAI-1 (p = 0.003). Furthermore, stage D COVID-19 patients had significantly higher tPA and TAFI values (p = 0.003). Conclusions: Hypofibrinolysis was the most prevalent condition among patients with severe COVID-19. In this study, several coagulation markers were elevated, making them suitable prognostic markers for hypofibrinolysis.

Designed and implemented over two decades ago, the Chronic Care Model is a well‐established chronic disease management framework that has steered several healthcare systems in successfully improving the clinical outcomes of patients with type 2 diabetes mellitus. Research evidence cements the role of the Chronic Care Model (with its six key elements of organization of healthcare delivery system, self‐management support, decision support, delivery system design, clinical information systems, and community resources and policies) as an integrated framework to revamp the type 2 diabetes mellitus‐related clinical practice and care that betters the patient care and clinical outcomes. The current review is an evidence‐lit summary of importance of use of Chronic Care Model in primary care and their impact on clinical outcomes for patients afflicted with one of the most debilitating metabolic diseases, type 2 diabetes mellitus.

Mutations within the hepatitis B virus surface antigen (HBsAg) were found to correlate with progressive liver diseases, including hepatocellular carcinoma (HCC). Mutations in this region can impact viral morphogenesis, virus-host interactions, and immune responses. In this cross-sectional study, we screened for mutations in the pre-S/S regions of HBsAg in sequences retrospectively generated from samples collected in Saudi Arabia. We analyzed 304 full-length HBsAg sequences isolated from samples collected from four clinical groups: inactive (n = 180), active (n = 62), liver cirrhosis (LC) (n = 36), and HCC (n = 26). Three mutations (N103D, Q30K, and I208T) in HBsAg showed significantly higher frequencies in the HCC group compared to other clinical groups. Additionally, the presence of the three mutations combined was significantly associated with HCC in a multivariate analysis. The evolutionary analysis further revealed that these mutation sites are subjected to positive selection within the HCC group. The structural analysis suggested that position 103 within HBsAg pre- S 1 region is prominently accessible and mutations at this site may disrupt interactions with viral/cellular factors or impact recognition by immune responses. Collectively, our findings highlight a significant increase in the frequency of three HBsAg mutations in a cohort of HCC patients in Saudi Arabia and their potential effect.