The pathogenesis of hemorrhagic fever with renal syndrome (HFRS) is greatly affected by different immune cells. At present, peripheral blood T cell receptor (TCR) or B cell receptor (BCR) library sequencing of HFRS is still lacking and expensive. In this study, the computational method TRUST4 was used to construct TCR and BCR libraries from a large number of RNA-seq data of peripheral blood of HFRS patients, and to analyze the clonality and diversity of disease immune libraries. Although the function of immune cells has been studied, the mechanism remains complex. The differentially expressed genes in each immune cell type and the cell-to-cell interactions between immune cell clusters have not been covered. In this work, we clustered 11 cell subsets from raw scRNA-seq data and disaggregated the characteristic changes in the proportion of cell subsets under disease conditions. CellChat, a cell-cell communication analysis tool, was also used to analyze the effects of MIF family, CD70 family, and GALECTIN family cytokines, which are reported to be involved in cell communication subsets, respectively. HDWGCNA analysis identified core genes involved in the occurrence and development of HFRS in T cells and B cells. The results of trajectory analysis showed that most cell subsets were in the developmental stage, transcription factors in Effector CD8+ T cells (GZMH), Effector CD8+ T cells (GZMK), It was highly expressed in Naive CD4+ T cells and Naive B cells. Our results comprehensively illustrated the dynamic changes of immune cells during the pathogenesis of HFRS. This work identifies specific V genes and J genes in TCR and BCR that can be used to extend our understanding of HFRS. These findings provide new insights into the diagnosis and treatment of this autoimmune disease.