Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 192, Issue 2, Pages 344-349Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/430953
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Funding
- NHLBI NIH HHS [R01 HL069413, R01 HL069413-08, HL69413] Funding Source: Medline
- NIAID NIH HHS [R21 AI046326, AI043279, R01 AI046326, R01 AI043279, AI046326, R37 AI046326] Funding Source: Medline
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Kawasaki disease (KD) is an enigmatic, self-limited vasculitis of childhood that is complicated by development of coronary-artery aneurysms. The high incidence of KD in Asian versus European populations prompted a search for genetic polymorphisms that are differentially distributed among these populations and that influence KD susceptibility. Here, we demonstrate a striking, inverse relationship between the worldwide distribution of CCR5-Delta 32 allele and the incidence of KD. In 164 KD patient-parent trios, 4 CCR5 haplotypes including the CCR5-Delta 32 allele were differentially transmitted from heterozygous parents to affected children. However, the magnitude of the reduced risk of KD associated with the CCR5-Delta 32 allele and certain CCR5 haplotypes was significantly greater in individuals who also possessed a high copy number of the gene encoding CCL3L1, the most potent CCR5 ligand. These findings, derived from the largest genetic study of any systemic vasculitis, suggest a central role of CCR5-CCL3L1 gene-gene interactions in KD susceptibility and the importance of gene modifiers in infectious diseases.
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