Nagasaka Miwako, Morioka Ichiro, Kawabata Akiko, Yamagishi Yoshiaki, Iwatani Sota, Taniguchi-Ikeda Mariko, Ishida Akihito, Iijima Kazumoto, Mori Yasuko
Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan; Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe, Japan.
Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan.
J Infect Chemother. 2016 Sep;22(9):593-8. doi: 10.1016/j.jiac.2016.05.010. Epub 2016 Jun 23.
Cytokines and chemokines induced by primary human herpes virus (HHV)-6B infection may play a critical role in the clinical manifestations of infection. In this study, we analyzed 40 cytokines/chemokines in febrile children with primary HHV-6B infection. Blood samples from 233 febrile and 36 afebrile patients 0-3 years of age were used for this study. In febrile patients, primary HHV-6B infection was determined by detection of HHV-6B DNA without anti-HHV-6 immunoglobulin G in the blood (HHV-6B group). Infection by other pathogens was assumed when HHV-6B DNA was not detected in the blood (non-HHV-6B group). Of the 233 febrile patients, 30 patients (13%) were diagnosed with primary HHV-6B infection. To analyze serum cytokines/chemokines, patients were randomly chosen from the HHV-6B (n = 25) and non-HHV-6B groups (n = 8). Sera from 25 afebrile patients were used as a control. When comparing the levels of 40 cytokines/chemokines between the HHV-6B and control groups, we found that four chemokines (chemokine [C-X-C motif] ligand [CXCL] 11, CXCL10, CXCL16, and chemokine [C-C motif] ligand [CCL] 2) were significantly upregulated in the HHV-6B group compared with those in the control. Of these, only CXCL11 levels were significantly higher in the HHV-6B group than in the non-HHV-6B group. Because the induction of CCL2 was already reported in an early study, we found, for the first time, the induction of three new chemokines, i.e., CXCL11, CXCL10, and CXCL16 in patients with primary HHV-6B infection. Importantly, we demonstrated that serum CXCL11 levels increased specifically in patients with HHV-6B infection.
原发性人疱疹病毒（HHV）-6B感染诱导的细胞因子和趋化因子可能在感染的临床表现中起关键作用。在本研究中，我们分析了原发性HHV-6B感染的发热儿童体内的40种细胞因子/趋化因子。本研究使用了233名0至3岁发热患者和36名无发热患者的血样。在发热患者中，通过检测血液中无抗HHV-6免疫球蛋白G的HHV-6B DNA来确定原发性HHV-6B感染（HHV-6B组）。当血液中未检测到HHV-6B DNA时，则假定为其他病原体感染（非HHV-6B组）。在233名发热患者中，30名患者（13%）被诊断为原发性HHV-6B感染。为了分析血清细胞因子/趋化因子，从HHV-6B组（n = 25）和非HHV-6B组（n = 8）中随机选择患者。将25名无发热患者的血清用作对照。在比较HHV-6B组和对照组之间40种细胞因子/趋化因子的水平时，我们发现与对照组相比，HHV-6B组中有四种趋化因子（趋化因子[C-X-C基序]配体[CXCL]11、CXCL10、CXCL16和趋化因子[C-C基序]配体[CCL]2）显著上调。其中，只有CXCL11水平在HHV-6B组中显著高于非HHV-6B组。由于早期研究中已经报道了CCL2的诱导，我们首次发现原发性HHV-6B感染患者中三种新趋化因子即CXCL11、CXCL10和CXCL16的诱导。重要的是，我们证明血清CXCL11水平在HHV-6B感染患者中特异性升高。
