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Association of ICAM3 genetic variant with severe acute respiratory syndrome
Authors
EYT Chan
JCK Chan
+23 more
KYK Chan
LC Chan
VSF Chan
ANY Cheung
JCY Ching
EYD Chow
CM Chu
PH Chung
FP Huang
US Khoo
ST Lai
GM Leung
SCL Lin
W Liu
HYS Ngan
M Peiris
P Sham
YQ Song
P Tam
ATY Wong
MS Xu
LYC Yam
SP Yip
Publication date
1 January 2007
Publisher
'University of Chicago Press'
Doi
Cite
Abstract
Genetic polymorphisms have been demonstrated to be associated with vulnerability to human infection. ICAM3, an intercellular adhesion molecule important for T cell activation, and FCER2 (CD23), an immune response gene, both located on chromosome 19p13.3, were investigated for host genetic susceptibility and association with clinical outcome. A case-control study based on 817 patients with confirmed severe acute respiratory syndrome (SARS), 307 health care worker control subjects, 290 outpatient control subjects, and 309 household control subjects unaffected by SARS from Hong Kong was conducted to test for genetic association. No significant association to susceptibility to SARS infection caused by the novel coronavirus (SARS-CoV) was found for the FCER2 and the ICAM3 single nucleotide polymorphisms. However, patients with SARS homozygous for ICAM3 Gly143 showed significant association with higher lactate dehydrogenase levels (P = .0067; odds ratio [OR], 4.31 [95% confidence interval {CI}, 1.37-13.56]) and lower total white blood cell counts (P = .022; OR, 0.30 [95% CI, 0.10-0.89]) on admission. These findings support the role of ICAM3 in the immunopathogenesis of SARS. © 2007 by the Infectious Diseases Society of America. All rights reserved.published_or_final_versio
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The Hong Kong Polytechnic University Pao Yue-kong Library
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