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用免疫组化酶杂技术检查了肾综合征出血热病毒（HFRSV）膜蛋白（MP）、核蛋白（NP）在患者外周血单个核细胞（PBMC）中的表达情况，同时用放免法检测了血浆内皮素（ET）、P物质（SP）、尿β2-微球蛋白（β2-m）及TH糖蛋白（THP）：发现HFRS患者从入院之日起至13病日在PBMC中均有MP与NP表达，但随首病情的好转表达强度逐渐减弱。血浆ET于入院初便见上升，低血压少尿期达高峰，多尿期以后渐恢复正常；血浆SP于病程前四期明显降低，使得ET／SP比值明显升高。病程中ET／SP比值与血尿素氮（BUN）及尿β2－m的变化曲线大体平行，与肌酐清除率（CCr）及尿THP变化情况完全相反。故认为PBMC也是HFRSV较常侵犯的靶细胞，且HFRSV可在其中复制增殖，并可向血管内皮细胞及其它组织扩散。单核-巨噬细胞激活后可释放其细胞因子加重血管损伤，后者释放内皮素可能是造成急性肾衰的重要因素。
The expression of membrane protein (MP) and nuclear protein (NP) of hemorrhagic fever with renal syndrome (HFRSV) in peripheral blood mononuclear cells (PBMCs) of patients with renal syndrome was examined by immunohistochemical enzyme hybridization technique. Plasma endothelin (ET), substance P (SP), urinary β2-microglobulin (β2-m) and TH glycoprotein (THP) were found in patients with HFRS from the date of admission to the 13th day in PBMC MP And NP expression, but with the improvement of the first condition, the expression intensity gradually weakened. The plasma ET increased at the beginning of admission, the peak of hypotension and oliguria reached its peak, and returned to normal after polyuria. Plasma SP significantly decreased in the first four stages of the course of disease, resulting in a significant increase in ET / SP ratio. The ET / SP ratio in the course of the disease was approximately parallel to the curve of BUN and β2-m, which was completely opposite to the changes of creatinine clearance (CCr) and urine THP. Therefore, PBMC is also considered as the target cell for HFRSV invasion. HFRSV can proliferate and proliferate into vascular endothelial cells and other tissues. Monocyte-macrophage activation can release cytokines to exacerbate vascular damage, which releases endothelin may be an important factor in causing acute renal failure.