Association of ICAM3 genetic variant with severe acute respiratory syndrome

KYK Chan, JCY Ching, MS Xu, Annie N.Y. Cheung, Shea Ping Yip, LYC Yam, ST Lai, CM Chu, ATY Wong, YQ Song, FP Huang, W Liu, PH Chung, GM Leung, EYD Chow, EYT Chan, JCK Chan, HYS Ngan, P Tam, LC ChanPak Chung Sham, VSF Chan, M Peiris, SCL Lin, Ui Soon Khoo

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)

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.
Original languageEnglish
Pages (from-to)271-280
Number of pages10
JournalJournal of Infectious Diseases
Volume196
Issue number2
DOIs
Publication statusPublished - 15 Jul 2007
Externally publishedYes

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