A deletion in the chemokine receptor 5 (CCR5) gene is associated with tickborne encephalitis

被引：154

作者：

Kindberg, Elin ^{[1
,2
]}

Mickiene, Aukse ^{[4
,5
,6
]}

Ax, Cecilia ^{[1
]}

Akerlind, Britt ^{[3
]}

Vene, Sirkka ^{[5
]}

Lindquist, Lars ^{[4
]}

Lundkvist, Ake ^{[5
]}

Svensson, Lennart ^{[1
,3
]}

机构：

[1] Linkoping Univ, Fac Med, Div Mol Virol, S-58185 Linkoping, Sweden

[2] Natl Board Forens Med, Dept Forens Genet, Linkoping, Sweden

[3] Linkoping Univ Hosp, Dept Clin Microbiol, S-58185 Linkoping, Sweden

[4] Karolinska Univ Hosp Huddinge, Karolinska Inst, Dept Med, Infect Dis Unit, Stockholm, Sweden

[5] Swedish Inst Infect Dis Control, Stockholm, Sweden

[6] Kaunas Univ Med, Clin Infect Dis, Kaunas, Lithuania

来源：

JOURNAL OF INFECTIOUS DISEASES | 2008年 / 197卷 / 02期

关键词：

D O I：

10.1086/524709

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Tickborne encephalitis (TBE) virus infections can be asymptomatic or cause moderate to severe injuries of the central nervous system. Why some individuals develop severe disease is unknown, but a role for host genetic factors has been suggested. To investigate whether chemokine receptor CCR5 is associated with TBE, CCR5 Delta 32 genotyping was performed among Lithuanian patients with TBE (n = 129) or with aseptic meningoencephalitis (n = 76) as well as among control subjects (n = 134). We found individuals homozygous for CCR5 Delta 32 (P = .026) only among patients with TBE and a higher allele prevalence among patients with TBE compared with the other groups studied. CCR5 Delta 32 allele prevalence also increased with the clinical severity of disease.

引用

页码：266 / 269

页数：4

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