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The global impact of the COVID-19 pandemic has been substantial. Emerging evidence underscores a strong clinical connection between COVID-19 and sepsis. Numerous studies have identified the unfolded protein response (UPR) pathway as a crucial pathogenic pathway for both COVID-19 and sepsis, but it remains to be investigated whether this signaling pathway operates as a common pathogenic mechanism for both COVID-19 and sepsis. In this study, single-cell RNA-seq data and transcriptome data for COVID-19 and sepsis cases were downloaded from GEO (Gene Expression Omnibus). By analyzing the single-cell transcriptome data, we identified B cells as the critical cell subset and the UPR pathway as the critical signaling pathway. Based on the transcriptome data, a machine learning diagnostic model was then constructed using the interleaved genes of B-cell-related and UPR-pathway-related genes. We validated the diagnostic model using both internal and external datasets and found the accuracy and stability of this model to be extremely strong. Even after integrating our algorithmic model with the patient's clinical status, it continued to yield identical results, further emphasizing the reliability of this model. This study provides a novel molecular perspective on the pathogenesis of sepsis and COVID-19 at the single-cell level and suggests that these two diseases may share a common mechanism. [ABSTRACT FROM AUTHOR]

To assess the relationship between the expression of CD38 and the progression of hemorrhagic fever with renal syndrome (HFRS), we determined the levels of CD38 during different phases of HFRS and evaluated the relationship between changes in CD38 expression and the progression of HFRS. The expression of CD38 in 68 patients with HFRS was analyzed by flow cytometry, and this method was also used to determine the levels of CD4+T, CD8+T, and B lymphocytes and NK cells. Furthermore, creatinine (Cr), uric acid (UA), and urea in serum at each stage of HFRS were measured using commercial kits. The basic clinical reference values for leukocytes, platelets (PLT), and red blood cells were determined by conventional methods. The colloidal gold method was used to measure HFRS antibody levels in the patients. A significant change in CD38 expression was observed from the fever phase to the recovery phase in patients with HFRS. Moreover, the expression of CD38 was proportionally correlated with the levels of Cr, UA, and urea in serum. In contrast, there was an inverse correlation between CD38 and PLT. Interestingly, an increase in CD38 expression correlated with an increase in CD8+T lymphocytes, B cells, and NK cells, but with a decrease in CD4+T lymphocytes. The expression of CD38 is associated with the progression of HFRS, suggesting that it may be a potent indicator of the stages of this disorder. [ABSTRACT FROM AUTHOR]