The genetic polymorphisms of HLA are strongly correlated with the disease severity after Hantaan virus infection in the Chinese Han population.

The genetic polymorphisms of HLA are strongly correlated with the disease severity after Hantaan virus infection in the Chinese Han population.
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HLA基因多态性与中国汉族人群感染汉滩病毒后病情严重程度密切相关。

DOI:
10.1155/2012/308237
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发表时间:
2012
影响因子:
--
通讯作者:
Jin B
Jin B
中科院分区:
其他
文献类型:
--
作者:
Ma Y;Yuan B;Yi J;Zhuang R;Wang J;Zhang Y;Xu Z;Zhang Y;Liu B;Wei C;Zhang C;Yang A;Jin B

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人类白细胞抗原(HLA)多态性是影响肾综合征出血热(HFRS)患者感染汉滩病毒(HTNV)后病情进展的遗传因素,目前对HLA多态性的认识还不完全。在本病例对照研究中,76例HFRS患者和370名健康对照者进行了HLA-A、-B和-DRB 1位点的分型。HLA-DRB 1位点的总体变异与HFRS的发病相关(P < 0.05)。HLA-DRB 1 - 09和HLA-B-46-DRB 1 - 09在肾综合征出血热患者中的分布频率明显增高。HLA-B等位基因51-DRB 1等位基因09与HFRS易感性相关(P = 0.037; OR = 3.62,95%CI:1.00-13.18)。HLA-B-46、HLA-B-46-DRB 1 - 09和HLA-B-51-DRB 1 - 09的频率在HFRS重症/危重患者中几乎都是增高的。HLA-B146-DRB 1 - 09(P = 0.011)、HLA-B151-DRB 1 - 09(P = 0.041)和HLA-B146(P = 0.011)阳性患者的最大血肌酐水平均高于阴性患者。提示HLA-B等位基因HLA-B146和HLA-B146-DRB 1109、HLA-B151-DRB 1109单倍型与HFRS病情加重和肾损害加重有关,这进一步加深了我们对HTNV感染不同结局的HLA多态性的认识。
The polymorphism of human leukocyte antigen (HLA), which is a genetic factor that influences the progression of hemorrhagic fever with renal syndrome (HFRS) after Hantaan virus (HTNV) infection, was incompletely understood. In this case-control study, 76 HFRS patients and 370 healthy controls of the Chinese Han population were typed for the HLA-A, -B, and -DRB1 loci. The general variation at the HLA-DRB1 locus was associated with the onset of HFRS (P < 0.05). The increasing frequencies of HLA-DRB1∗09 and HLA-B∗46-DRB1∗09 in HFRS patients were observed as reproducing a previous study. Moreover, the HLA-B∗51-DRB1∗09 was susceptible to HFRS (P = 0.037; OR = 3.62; 95% CI: 1.00–13.18). The increasing frequencies of HLA-B∗46, HLA-B∗46-DRB1∗09, and HLA-B∗51-DRB1∗09 were observed almost in severe/critical HFRS patients. The mean level of maximum serum creatinine was higher in HLA-B∗46-DRB1∗09 (P = 0.011), HLA-B∗51-DRB1∗09 (P = 0.041), or HLA-B∗46 (P = 0.011) positive patients than that in the negative patients. These findings suggest that the allele HLA-B∗46 and haplotypes HLA-B∗46-DRB1∗09 and HLA-B∗51-DRB1∗09 in patients could contribute to a more severe degree of HFRS and more serious kidney injury, which improve our understanding of the HLA polymorphism for a different outcome of HTNV infection.
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