Hantaan virus infection may cause severe lethal hemorrhagic fever with renal syndrome (HFRS) in humans. The chemokine fractalkine (CX3CL1) acts as a proinflammatory cytokine, and it is elevated in several infectious diseases. However, little is known about the contributions of CX3CL1 to HFRS pathogenesis. Present study detected plasma CX3CL1 levels and expression of the receptor CX3CR1 in HFRS patients and discussed the possible effects of CX3CL1 on pathogenesis of HFRS. Plasma CX3CL1 in acute phase and Critical/Severe groups of HFRS patients were significantly increased compared to that in normal controls (p < 0.001 and p < 0.01, respectively). High plasma CX3CL1 was negatively correlated with platelet count (r = −0.5844, p < 0.0001) and positively correlated with blood urea nitrogen (r = 0.3668, p = 0.0039), creatinine (r = 0.42, p = 0.0008), and white blood cells (r = 0.2646, p = 0.0411). Expression of CX3CR1 on nonclassical and intermediate monocytes was also increased in the acute phase (p < 0.01 for both the cells) and Critical/Severe groups (p < 0.05 and p < 0.01, respectively) of HFRS patients compared to that in normal controls. Taken together, elevation of plasma CX3CL1 in HFRS patients and expression of CX3CR1 on nonclassical and intermediate monocyte subsets might provide new insights into the potential role of CX3CL1/CX3CR1 in pathogenesis of HFRS.

中文翻译：

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血浆 Fractalkine 水平升高与人类肾综合征出血热的严重程度有关

汉坦病毒感染可能会导致人类出现严重的致命性肾综合征出血热 (HFRS)。趋化因子fractalkine (CX3CL1) 作为一种促炎细胞因子，在几种传染病中升高。然而，关于 CX3CL1 对 HFRS 发病机制的贡献知之甚少。本研究检测了 HFRS 患者血浆 CX3CL1 水平和受体 CX3CR1 的表达，并讨论了 CX3CL1 对 HFRS 发病机制的可能影响。与正常对照组相比，HFRS 患者急性期和危重/重度组的血浆 CX3CL1 显着升高（分别为p  < 0.001 和p  < 0.01）。高血浆 CX3CL1 与血小板计数呈负相关 ( r  = -0.5844, p < 0.0001) 并与血尿素氮 ( r  = 0.3668, p  = 0.0039)、肌酐 ( r  = 0.42, p  = 0.0008) 和白细胞 ( r  = 0.2646, p  = 0.0411) 呈正相关。CX3CR1 在非经典和中间单核细胞上的表达在急性期（两个细胞的p  < 0.01）和严重/严重组（p  < 0.05 和p < 0.01，分别）HFRS 患者与正常对照组相比。总之，HFRS 患者血浆 CX3CL1 的升高和 CX3CR1 在非经典和中间单核细胞亚群上的表达可能为 CX3CL1/CX3CR1 在 HFRS 发病机制中的潜在作用提供新的见解。