Epstein-Barr virus (EBV) is a risk factor for diffuse large B-cell lymphoma (DLBCL) and systemic lupus erythematosus (SLE). While prior research has suggested a potential correlation between SLE and DLBCL, the molecular mechanisms remain unclear. The present study aimed to explore the contribution of EBV infection to the pathogenesis of DLBCL in the individuals with SLE using bioinformatics approaches. The Gene Expression Omnibus database was used to compile the gene expression profiles of EBV-infected B cells (GSE49628), SLE (GSE61635), and DLBCL (GSE32018). Altogether, 72 shared common differentially expressed genes (DEGs) were extracted and enrichment analysis of the shared genes showed that p53 signaling pathway was a common feature of the pathophysiology. Six hub genes were selected using protein–protein interaction (PPI) network analysis, including CDK1, KIF23, NEK2, TOP2A, NEIL3 and DEPDC1, which showed preferable diagnostic values for SLE and DLBCL and involved in immune cell infiltration and immune responses regulation. Finally, TF-gene and miRNA-gene regulatory networks and 10 potential drugs molecule were predicted. Our study revealed the potential molecular mechanisms by which EBV infection contribute to the susceptibility of DLBCL in SLE patients for the first time and identified future biomarkers and therapeutic targets for SLE and DLBCL.

Respiratory tract infections (RTIs) are among the most prevalent diseases in human society and pose a major global health threat, affecting millions annually. A wide range of pathogens, primarily viruses and bacteria, cause RTIs. These infections often present with similar symptoms, which limits effective clinical treatment. Extensive research has addressed RTIs, with ongoing discussion regarding their current status and advancements in detection technologies. Novel laboratory methods that offer rapid, sensitive, and specific results now supplement traditional diagnostic approaches. In this review, we summarize the infection characteristics and detection methods of common respiratory pathogens, evaluate the effectiveness and limitations of current detection methods, and aim to promote advancements in laboratory diagnosis and explore the potential of emerging technologies in this field.

Nasopharyngeal carcinoma (NPC) is a malignant tumor prevalent in Southern China, strongly associated with Epstein-Barr virus (EBV) infection. Accurate diagnosis is critical in determining treatment strategies for NPC. In clinical practice, imaging techniques are the most predominant diagnostic methods, which are costly and may fail to detect small metastatic lesions. Moreover, while EBV antibody and DNA tests contribute to the assessment of tumor progression, they carry the risk of false negatives. To develop novel serum protein biomarkers for late-stage NPC diagnosis, our study included 189 samples, including healthy controls (HCs) and early- or late-stage NPC patients. A high-throughput serum proteomics approach was employed to delineate protein profiles, followed by enzyme-linked immunosorbent assay (ELISA) validation of candidate biomarkers. Our study identified fibronectin 1 (FN1) as a promising serum biomarker for late-stage NPC. The serum levels of FN1 significantly decreased with tumor progression, achieving AUCs of 0.71 and 0.72 in differentiating late-stage NPC patients from HCs and early-stage NPC patients, respectively. Importantly, FN1 demonstrated diagnostic utility in challenging cases, accurately identifying all VCA-IgA-negative and 88.2% EBV DNA-negative patients with late-stage NPC. Combining FN1 with VCA-IgA or EBV DNA test significantly increased diagnostic sensitivity for advanced NPC. Our discovery of FN1 as a biomarker for the late-stage diagnosis of NPC will assist in clinical treatment decisions and improve the prognosis of patients.

Introduction: Nasopharyngeal carcinoma (NPC), one of the most common malignancies of the head and neck, is characterised by a complex pathogenesis and an unfavourable prognosis. Recently, disulfidoptosis, a novel form of cell death, has been proposed. Several studies in recent years have extensively investigated the function of the disulfidoptosis-related SLC7A11 gene in cancer, but the role of its partner protein, SLC3A2, remains unknown unclear in NPC.Methods: GEO database analysis confirmed SLC3A2's prognostic impact on nasopharyngeal carcinoma. ROC, Kaplan-Meier analyses, and stage-specific expression studies showed a strong correlation with poor HNSC prognosis. GO and KEGG analyses pinpointed relevant signaling pathways. In vitro, SLC3A2's influence on cell proliferation, migration, and invasion was evaluated through CCK8, wound healing, colony formation, transwell assays, and cell cycle analysis.Results: In this study, we identified the high expression of SLC3A2 in NPC and head and neck squamous cell carcinoma (HNSC) and analyzed its potential mechanism and correlation with patient prognosis. Furthermore, a negative relationship was found between the expression level of SLC3A2 and the extent of immune cell infiltration and immune checkpoint. Differentially expressed genes (DEGs) between the high and low SLC3A2 expression groups were primarily involved in cytokine-cytokine receptor interaction and immune response. Finally, in vitro experiments demonstrated that SLC3A2 stimulates tumor cell proliferation and migration. Discussion: In conclusion, these results indicated a strong association between SLC3A2 and progression in both NPC and HNSC, suggesting it as a promising biomarker for predicting adverse prognosis in NPC and HNSC patients.