Genetic deficiency of chemokine receptor CCR5 is a strong risk factor for symptomatic West Nile Virus infection: A meta-analysis of 4 cohorts in the US epidemic

被引:154
作者
Lim, Jean K. [1 ]
Louie, Christine Y. [1 ]
Glaser, Carol [2 ]
Jean, Cynthia [2 ]
Johnson, Bernard [3 ]
Johnson, Hope [3 ]
McDermott, David H. [1 ]
Murphy, Philip M. [1 ]
机构
[1] NIAID, Mol Signaling Sect, Lab Mol Immunol, Natl Inst Hlth, Bethesda, MD 20892 USA
[2] Calif Dept Hlth Serv, Viral & Rickettsial Dis Lab, Richmond, CA USA
[3] Illinois Dept Publ Hlth, Div Labs, Chicago, IL USA
关键词
D O I
10.1086/524691
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
West Nile virus (WNV) causes disease in similar to 20% of infected humans. We previously reported that homozygosity for CCR5 Delta 32, a nonfunctional variant of chemokine receptor CCR5, is markedly increased among symptomatic WNV-seropositive patients from Arizona and Colorado. To confirm this, we analyzed cohorts from California and Illinois. An increase in CCR5-deficient subjects was found in both (for California, , lodds ratio [OR], 4.2 [95% confidence interval {CI}, 1.5-11.9] [P= .004]; for Illinois, OR, 3.1 [95% CI, 0.9-11.2] [P = .06]). A meta-analysis of all 4 cohorts showed an OR of 4.2 (95% CI, 2.1-8.3 [P < .0001]). Thus, CCR5 deficiency is a strong and consistent risk factor for symptomatic WNV infection in the United States.
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页码:262 / 265
页数:4
相关论文
共 15 条
[1]  
Abdi R, 2002, J AM SOC NEPHROL, V13, DOI 10.1681/ASN.V133754
[2]   Chemokine receptor CCR5 promotes leukocyte trafficking to the brain and survival in West Nile virus infection [J].
Glass, WG ;
Lim, JK ;
Cholera, R ;
Pletnev, AG ;
Gao, JL ;
Murphy, PM .
JOURNAL OF EXPERIMENTAL MEDICINE, 2005, 202 (08) :1087-1098
[3]   CCR5 deficiency increases risk of symptomatic West Nile virus infection [J].
Glass, WG ;
McDermott, DH ;
Lim, JK ;
Lekhong, S ;
Yu, SF ;
Frank, WA ;
Pape, J ;
Cheshier, RC ;
Murphy, PM .
JOURNAL OF EXPERIMENTAL MEDICINE, 2006, 203 (01) :35-40
[4]   West Nile virus: Epidemiology and clinical features of an emerging epidemic in the United States [J].
Hayes, EB ;
Gubler, DJ .
ANNUAL REVIEW OF MEDICINE, 2006, 57 :181-194
[5]   Replication validity of genetic association studies [J].
Ioannidis, JPA ;
Ntzani, EE ;
Trikalinos, TA ;
Contopoulos-Ioannidis, DG .
NATURE GENETICS, 2001, 29 (03) :306-309
[6]   Neuronal CXCL10 directs CD8+ T-cell recruitment and control of West Nile virus encephalitis [J].
Klein, RS ;
Lin, E ;
Zhang, B ;
Luster, AD ;
Tollett, J ;
Samuel, MA ;
Engle, M ;
Diamond, MS .
JOURNAL OF VIROLOGY, 2005, 79 (17) :11457-11466
[7]   Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States [J].
Lanciotti, RS ;
Roehrig, JT ;
Deubel, V ;
Smith, J ;
Parker, M ;
Steele, K ;
Crise, B ;
Volpe, KE ;
Crabtree, MB ;
Scherret, JH ;
Hall, RA ;
MacKenzie, JS ;
Cropp, CB ;
Panigrahy, B ;
Ostlund, E ;
Schmitt, B ;
Malkinson, M ;
Banet, C ;
Weissman, J ;
Komar, N ;
Savage, HM ;
Stone, W ;
McNamara, T ;
Gubler, DJ .
SCIENCE, 1999, 286 (5448) :2333-2337
[8]   CCR5: no longer a 'good for nothing' gene - chemokine control of West Nile virus infection [J].
Lim, Jean K. ;
Glass, William G. ;
McDermott, David H. ;
Murphy, Philip M. .
TRENDS IN IMMUNOLOGY, 2006, 27 (07) :308-312
[9]   Global distribution of the CCR5 gene 32-basepair deletion [J].
Martinson, JJ ;
Chapman, NH ;
Rees, DC ;
Liu, YT ;
Clegg, JB .
NATURE GENETICS, 1997, 16 (01) :100-103
[10]   A nonsense mutation in the gene encoding 2′-5′-oligoadenylate synthetase/L1 isoform is associated with West Nile virus susceptibility in laboratory mice [J].
Mashimo, T ;
Lucas, M ;
Simon-Chazottes, D ;
Frenkiel, MP ;
Montagutelli, X ;
Ceccaldi, PE ;
Deubel, V ;
Guénet, JL ;
Deprès, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (17) :11311-11316