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2
Virus RNA Load in Patients with Tick-Borne Encephalitis, Slovenia.斯洛文尼亚蜱传脑炎患者的病毒 RNA 载量。
Emerg Infect Dis. 2018 Jul;24(7):1315-1323. doi: 10.3201/eid2407.180059.
3
Epidemiological patterns of tick-borne encephalitis in Lithuania and clinical features in adults in the light of the high incidence in recent years: a retrospective study.近年来发病率升高背景下的立陶宛蜱传脑炎的流行病学模式和成人临床特征:一项回顾性研究。
Eur J Neurol. 2018 Feb;25(2):268-274. doi: 10.1111/ene.13486. Epub 2017 Dec 6.
4
Analysis of the relationship between single nucleotide polymorphism of the CD209, IL-10, IL-28 and CCR5 D32 genes with the human predisposition to developing tick-borne encephalitis.分析CD209、IL-10、IL-28和CCR5 D32基因单核苷酸多态性与人类感染蜱传脑炎易感性之间的关系。
Postepy Hig Med Dosw (Online). 2017 Jan 4;71(1):788-796. doi: 10.5604/01.3001.0010.3856.
5
Comparative analysis of complete genome sequences of European subtype tick-borne encephalitis virus strains isolated from Ixodes persulcatus ticks, long-tailed ground squirrel (Spermophilus undulatus), and human blood in the Asian part of Russia.对从俄罗斯亚洲部分的全沟硬蜱、长尾黄鼠(草原黄鼠)和人血液中分离出的欧洲亚型蜱传脑炎病毒株的全基因组序列进行比较分析。
Ticks Tick Borne Dis. 2017 Jun;8(4):547-553. doi: 10.1016/j.ttbdis.2017.03.002. Epub 2017 Mar 9.
6
Dual Function of Ccr5 during Langat Virus Encephalitis: Reduction in Neutrophil-Mediated Central Nervous System Inflammation and Increase in T Cell-Mediated Viral Clearance.Ccr5在兰加特病毒脑炎中的双重作用:减少中性粒细胞介导的中枢神经系统炎症并增加T细胞介导的病毒清除
J Immunol. 2016 Jun 1;196(11):4622-31. doi: 10.4049/jimmunol.1502452. Epub 2016 Apr 29.
7
The expression of the chemokine receptor CCR5 in tick-borne encephalitis.趋化因子受体CCR5在蜱传脑炎中的表达。
J Neuroinflammation. 2016 Feb 22;13:45. doi: 10.1186/s12974-016-0511-0.
8
Tick-borne encephalitis: A review of epidemiology, clinical characteristics, and management.蜱传脑炎:流行病学、临床特征及管理综述
World J Clin Cases. 2015 May 16;3(5):430-41. doi: 10.12998/wjcc.v3.i5.430.
9
Analysis of serum levels of cytokines, chemokines, growth factors, and monoamine neurotransmitters in patients with tick-borne encephalitis: identification of novel inflammatory markers with implications for pathogenesis.分析蜱传脑炎患者血清细胞因子、趋化因子、生长因子和单胺神经递质水平:发现新的炎症标志物,对发病机制具有启示意义。
J Med Virol. 2015 May;87(5):885-92. doi: 10.1002/jmv.24140. Epub 2015 Feb 11.
10
Polymorphisms in chemokine receptor 5 and Toll-like receptor 3 genes are risk factors for clinical tick-borne encephalitis in the Lithuanian population.趋化因子受体5和Toll样受体3基因的多态性是立陶宛人群临床蜱传脑炎的危险因素。
PLoS One. 2014 Sep 16;9(9):e106798. doi: 10.1371/journal.pone.0106798. eCollection 2014.

波兰人群中CCR5基因型与蜱传脑炎临床表现及发病率之间不存在关联

The Lack of the Association of the CCR5 Genotype with the Clinical Presentation and Frequency of Tick-Borne Encephalitis in the Polish Population.

作者信息

Grygorczuk Sambor, Dunaj-Małyszko Justyna, Sulik Artur, Toczyłowski Kacper, Czupryna Piotr, Żebrowska Agnieszka, Parczewski Miłosz

机构信息

Department of the Infectious Diseases and Neuroinfections, Faculty of Medicine, Medical University of Białystok, ul. Żurawia 14, 15-540 Białystok, Poland.

Department of the Pediatric Infectious Diseases, Faculty of Medicine, Medical University of Białystok, ul. Jerzego Waszyngtona 17, 15-274 Białystok, Poland.

出版信息

Pathogens. 2022 Mar 4;11(3):318. doi: 10.3390/pathogens11030318.

DOI:10.3390/pathogens11030318
PMID:35335642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8955457/
Abstract

BACKGROUND

The host factors influencing the susceptibility to and the severity of tick-borne encephalitis (TBE) are poorly defined. The loss-of-function mutation in the chemokine receptor gene was identified as a risk factor for West Nile encephalitis and possibly for TBE, suggesting a protective role of CCR5 in encephalitis.

METHODS

We studied the genotype in 205 TBE patients stratified by a clinical presentation and 257 controls from the same endemic area (Podlasie, Poland). The genotype distribution between the groups and differences between TBE patients with different genotypes were analyzed.

RESULTS

There were 36 (17.6%) heterozygotes and 3 (1.5%) homozygotes in the TBE group, with no statistically significant difference in comparison with the controls. The allele did not associate with the clinical presentation or the severity of TBE. The cerebrospinal fluid (CSF) inflammatory parameters did not differ between the wild-type () and genotype patients. The TBE clinical presentation and CSF parameters in three homozygotes were unremarkable.

CONCLUSIONS

The lack of association of with the risk and clinical presentation of TBE challenges the suspected CCR5 protective role. CCR5 is not indispensable for the effective immune response against the TBE virus.

摘要

背景

影响蜱传脑炎(TBE)易感性和严重程度的宿主因素尚不清楚。趋化因子受体基因的功能丧失突变被确定为西尼罗河脑炎的危险因素,也可能是TBE的危险因素,提示CCR5在脑炎中具有保护作用。

方法

我们研究了205例按临床表现分层的TBE患者和来自同一流行地区(波兰波德拉谢)的257例对照者的CCR5基因型。分析了两组之间的基因型分布以及不同基因型TBE患者之间的差异。

结果

TBE组中有36例(17.6%)杂合子和3例(1.5%)纯合子,与对照组相比无统计学显著差异。CCR5等位基因与TBE的临床表现或严重程度无关。野生型(CCR5+/+)和CCR5基因型患者的脑脊液(CSF)炎症参数无差异。3例CCR5纯合子患者的TBE临床表现和CSF参数无异常。

结论

CCR5与TBE风险和临床表现缺乏关联,这对CCR5的推测性保护作用提出了挑战。CCR5对于针对TBE病毒的有效免疫反应并非不可或缺。