Thus, despite the involvement of different IFNs in the pathophysiology of RSV infection, genetic variants in IFNG and related genes might not alter the risk for the development of severe RSV-associated diseases.
Both the homozygous hyporesponsive 299Gly genotype of TLR4 and the non-synonymous SP-A and SP-D polymorphism influence the presentation of RSV infection.
To assess, by a candidate-gene approach, whether genetic polymorphisms in IL-4/IL-13 pathway are associated with RSV infection severity and its outcome in Chilean children.
By investigating IL4 and IL13 polymorphisms in 131 children with severe RSV infection and 270 control subjects, we found an association between IL13 polymorphism -1112C/T and severe RSV infection (P = .026).
Furthermore, haplotypes analysis of the two TLR4 polymorphisms by three independent programs revealed association of haplotypes with severe RSV infection (p<or= 0.0010).
Two independent populations of infants with RSV bronchiolitis revealed that the severity of RSV infection is determined by the TLR4 genotype of the individual and by environmental exposure to LPS.
To conclude, we could not replicate the previously reported association with SNPs in the IL4 and IL4R genes in our independent cohort, nor did we find that common SNPs in genes encoding for RLRs and the downstream adapter MAVS were associated with susceptibility to severe RSV infections.
To assess, by a candidate-gene approach, whether genetic polymorphisms in IL-4/IL-13 pathway are associated with RSV infection severity and its outcome in Chilean children.
Because SP-A and SP-D act directly in the clearance of common lung pathogens, the genes encoding these proteins have been implicated as candidates in a few infectious diseases, including respiratory syncytial virus (RSV) infections and tuberculosis.
Both the homozygous hyporesponsive 299Gly genotype of TLR4 and the non-synonymous SP-A and SP-D polymorphism influence the presentation of RSV infection.
Because SP-A and SP-D act directly in the clearance of common lung pathogens, the genes encoding these proteins have been implicated as candidates in a few infectious diseases, including respiratory syncytial virus (RSV) infections and tuberculosis.
Both the homozygous hyporesponsive 299Gly genotype of TLR4 and the non-synonymous SP-A and SP-D polymorphism influence the presentation of RSV infection.
Because SP-A and SP-D act directly in the clearance of common lung pathogens, the genes encoding these proteins have been implicated as candidates in a few infectious diseases, including respiratory syncytial virus (RSV) infections and tuberculosis.
Hence, we provide mechanistic insight that the FokI VDR polymorphism renders STAT1-mediated antiviral immune reactions to RSV infection non-responsive to vitamin D control, resulting in enhanced immunopathology and exacerbated RSV bronchiolitis.