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Article: Functional variants regulating LGALS1 (Galectin 1) expression affect human susceptibility to influenza A(H7N9)

TitleFunctional variants regulating LGALS1 (Galectin 1) expression affect human susceptibility to influenza A(H7N9)
Authors
Issue Date2015
Citation
Scientific Reports, 2015, v. 5 How to Cite?
AbstractThe fatality of avian influenza A(H7N9) infection in humans was over 30%. To identify human genetic susceptibility to A(H7N9) infection, we performed a genome-wide association study (GWAS) involving 102 A(H7N9) patients and 106 heavily-exposed healthy poultry workers, a sample size critically restricted by the small number of human A(H7N9) cases. To tackle the stringent significance cutoff of GWAS, we utilized an artificial imputation program SnipSnip to improve the association signals. In single-SNP analysis, one of the top SNPs was rs13057866 of LGALS1. The artificial imputation (AI) identified three non-genotyped causal variants, which can be represented by three anchor/partner SNP pairs rs13057866/rs9622682 (AI P = 1.81 × 10-7), rs4820294/rs2899292 (2.13 × 10-7) and rs62236673/rs2899292 (4.25 × 10-7) respectively. Haplotype analysis of rs4820294 and rs2899292 could simulate the signal of a causal variant. The rs4820294/rs2899292 haplotype GG, in association with protection from A(H7N9) infection (OR = 0.26, P = 5.92 × 10-7) correlated to significantly higher levels of LGALS1 mRNA (P = 0.050) and protein expression (P = 0.025) in lymphoblast cell lines. Additionally, rs4820294 was mapped as an eQTL in human primary monocytes and lung tissues. In conclusion, functional variants of LGALS1 causing the expression variations are contributable to the differential susceptibility to influenza A(H7N9).
Persistent Identifierhttp://hdl.handle.net/10722/222679
ISSN
2015 Impact Factor: 5.228
2015 SCImago Journal Rankings: 2.073
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChen, Yu-
dc.contributor.authorZhou, Jie-
dc.contributor.authorCheng, Zhongshan-
dc.contributor.authorYang, Shigui-
dc.contributor.authorChu, Hin-
dc.contributor.authorFan, Yanhui-
dc.contributor.authorLi, Cun-
dc.contributor.authorWong, Bosco Ho Yin-
dc.contributor.authorZheng, Shufa-
dc.contributor.authorZhu, Yixin-
dc.contributor.authorYu, Fei-
dc.contributor.authorWang, Yiyin-
dc.contributor.authorLiu, Xiaoli-
dc.contributor.authorGao, Hainv-
dc.contributor.authorYu, Liang-
dc.contributor.authorTang, Linglin-
dc.contributor.authorCui, Dawei-
dc.contributor.authorHao, Ke-
dc.contributor.authorBossé, Yohan-
dc.contributor.authorObeidat, Ma'en-
dc.contributor.authorBrandsma, Corry Anke-
dc.contributor.authorSong, You Qiang-
dc.contributor.authorTo, Kelvin Kai Wang-
dc.contributor.authorSham, Pak Chung-
dc.contributor.authorYuen, Kwok Yung-
dc.contributor.authorLi, Lanjuan-
dc.date.accessioned2016-01-19T03:36:55Z-
dc.date.available2016-01-19T03:36:55Z-
dc.date.issued2015-
dc.identifier.citationScientific Reports, 2015, v. 5-
dc.identifier.issn2045-2322-
dc.identifier.urihttp://hdl.handle.net/10722/222679-
dc.description.abstractThe fatality of avian influenza A(H7N9) infection in humans was over 30%. To identify human genetic susceptibility to A(H7N9) infection, we performed a genome-wide association study (GWAS) involving 102 A(H7N9) patients and 106 heavily-exposed healthy poultry workers, a sample size critically restricted by the small number of human A(H7N9) cases. To tackle the stringent significance cutoff of GWAS, we utilized an artificial imputation program SnipSnip to improve the association signals. In single-SNP analysis, one of the top SNPs was rs13057866 of LGALS1. The artificial imputation (AI) identified three non-genotyped causal variants, which can be represented by three anchor/partner SNP pairs rs13057866/rs9622682 (AI P = 1.81 × 10-7), rs4820294/rs2899292 (2.13 × 10-7) and rs62236673/rs2899292 (4.25 × 10-7) respectively. Haplotype analysis of rs4820294 and rs2899292 could simulate the signal of a causal variant. The rs4820294/rs2899292 haplotype GG, in association with protection from A(H7N9) infection (OR = 0.26, P = 5.92 × 10-7) correlated to significantly higher levels of LGALS1 mRNA (P = 0.050) and protein expression (P = 0.025) in lymphoblast cell lines. Additionally, rs4820294 was mapped as an eQTL in human primary monocytes and lung tissues. In conclusion, functional variants of LGALS1 causing the expression variations are contributable to the differential susceptibility to influenza A(H7N9).-
dc.languageeng-
dc.relation.ispartofScientific Reports-
dc.titleFunctional variants regulating LGALS1 (Galectin 1) expression affect human susceptibility to influenza A(H7N9)-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1038/srep08517-
dc.identifier.pmid25687228-
dc.identifier.scopuseid_2-s2.0-84923355610-
dc.identifier.hkuros246444-
dc.identifier.volume5-
dc.identifier.eissn2045-2322-
dc.identifier.isiWOS:000349456600007-

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