tetano
Editor, Senior Moderator
Eur Respir J. 2011 Jul 7. [Epub ahead of print]
Genetic variants associated with severe pneumonia in A/H1N1 influenza infection.
Z??iga J, Buend?a I, Zhao Y, Jim?nez L, Torres D, Romo J, Ram?rez G, Cruz A, Vargas-Alarcon G, Sheu CC, Chen F, Su L, Tager AM, Pardo A, Selman M, Christiani DC.
Source
M?xico D.F., Mexico.
Abstract
The A/H1N1 influenza strain isolated in Mexico in 2009 caused severe pulmonary illness in a small number of exposed individuals. Our objective was to determine the influence of genetic factors on their susceptibility. We carried out a case-control association study genotyping 91 patients with confirmed severe pneumonia from A/H1N1 infection and 98 exposed but asymptomatic household contacts using the HumanCVD BeadChip (Illumina). Four risk SNPs were significantly (p<0.0001) associated with severe pneumonia: rs1801274 [Fc fragment of IgG, low affinity IIA, receptor (FCGR2A) gene, chromosome 1, OR=2.68, 95%CI=1.69-4.25]; rs9856661 (gene unknown, chromosome 3, OR=2.62, 95%CI=1.64-4.18); rs8070740 [RPA interacting protein (RPAIN) gene, chromosome 17, OR=2.67, 95%CI=1.63-4.39], and rs3786054 [complement component 1, q subcomponent binding protein (C1QBP) gene, chromosome 17, OR=3.13, 95%CI=1.89-5.17]. All SNP's remained significant after adjustment for gender and comorbidities. The SNPs on chromosome 17 were in linkage disequilibrium. These findings revealed that gene polymorphisms located in chromosomes 1 and 17 might influence susceptibility to development of severe pneumonia in A/H1N1 infection. Two of these SNPs are mapped within genes (FCGR2A, C1QBP) involved in the handling of immune complexes and complement activation respectively, suggesting that these genes may confer risk due to increased activation of host immunity.
PMID:
21737555
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21737555
Genetic variants associated with severe pneumonia in A/H1N1 influenza infection.
Z??iga J, Buend?a I, Zhao Y, Jim?nez L, Torres D, Romo J, Ram?rez G, Cruz A, Vargas-Alarcon G, Sheu CC, Chen F, Su L, Tager AM, Pardo A, Selman M, Christiani DC.
Source
M?xico D.F., Mexico.
Abstract
The A/H1N1 influenza strain isolated in Mexico in 2009 caused severe pulmonary illness in a small number of exposed individuals. Our objective was to determine the influence of genetic factors on their susceptibility. We carried out a case-control association study genotyping 91 patients with confirmed severe pneumonia from A/H1N1 infection and 98 exposed but asymptomatic household contacts using the HumanCVD BeadChip (Illumina). Four risk SNPs were significantly (p<0.0001) associated with severe pneumonia: rs1801274 [Fc fragment of IgG, low affinity IIA, receptor (FCGR2A) gene, chromosome 1, OR=2.68, 95%CI=1.69-4.25]; rs9856661 (gene unknown, chromosome 3, OR=2.62, 95%CI=1.64-4.18); rs8070740 [RPA interacting protein (RPAIN) gene, chromosome 17, OR=2.67, 95%CI=1.63-4.39], and rs3786054 [complement component 1, q subcomponent binding protein (C1QBP) gene, chromosome 17, OR=3.13, 95%CI=1.89-5.17]. All SNP's remained significant after adjustment for gender and comorbidities. The SNPs on chromosome 17 were in linkage disequilibrium. These findings revealed that gene polymorphisms located in chromosomes 1 and 17 might influence susceptibility to development of severe pneumonia in A/H1N1 infection. Two of these SNPs are mapped within genes (FCGR2A, C1QBP) involved in the handling of immune complexes and complement activation respectively, suggesting that these genes may confer risk due to increased activation of host immunity.
PMID:
21737555
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21737555