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Evidence suggests that Toll-like receptor 4 (TLR4) contributes to immune recognition of respiratory syncytial virus (RSV). The TLR4 gene harbours a polymorphism-Asp299Gly-previously associated with reduced TLR4 signalling. To understand of how host genetic variation influences the outcome of RSV infection in children, we examined the association between the TLR4 299Gly allele and severe RSV disease. By genotyping 236 children with RSV infection and 219 healthy controls we found no association between the risk of severe RSV infection and Asp299Gly polymorphisms (P>0.05), and we demonstrate that the TLR4 Asp299Gly genotype does not influence susceptibility to either RSV serotype A or B (P>0.05). Finally, examining the functional impact of the TLR4 Asp299Gly polymorphism (n=58), we demonstrate that proinflammatory cytokine production following TLR4 activation was indistinguishable between homozygous (Asp/Asp) and heterozygous (Asp/Gly) subjects. We conclude that the Asp299Gly TLR4 polymorphism does not alter receptor function and does not influence the risk of severe RSV infection.

Original publication

DOI

10.1016/j.clim.2007.03.003

Type

Journal article

Journal

Clinical immunology (Orlando, Fla.)

Publication Date

06/2007

Volume

123

Pages

252 - 257

Addresses

Department of Pediatrics, BC Children’s Hospital, Child & Family Research Institute, University of British Columbia, Vancouver, BC, Canada.

Keywords

Leukocytes, Mononuclear, Humans, Respiratory Syncytial Virus, Human, Respiratory Syncytial Virus Infections, Genetic Predisposition to Disease, Lipopolysaccharides, Tumor Necrosis Factor-alpha, Interleukin-6, Risk Factors, Gene Frequency, Genotype, Polymorphism, Single Nucleotide, Adolescent, Child, Child, Preschool, Infant, Infant, Newborn, Female, Male, Toll-Like Receptor 4, Interleukin-1beta