Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/34790
Title: Association of ICAM3 genetic variant with severe acute respiratory syndrome
Authors: Chan, KYK
Ching, JCY
Xu, MS
Cheung, ANY
Yip, SP 
Yam, LYC
Lai, ST
Chu, CM
Wong, ATY
Song, YQ
Huang, FP
Liu, W
Chung, PH
Leung, GM
Chow, EY
Chan, EY
Chan, JY
Ngan, HY
Tam, P
Chan, LC
Sham, P
Chan, VS
Peiris, M
Lin, SC
Khoo,US
Issue Date: 2007
Publisher: Oxford University Press
Source: Journal of infectious disease, 2007, v. 196, no. 2, p. 271-280 How to cite?
Journal: Journal of infectious disease
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-CoV infection 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.
URI: http://hdl.handle.net/10397/34790
ISSN: 0022-1899
DOI: 10.1086/518892
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