Our findings support the hypothesis of the pivotal role of the G glycoprotein CX3CR1 pathway in the pathogenesis of RSV bronchiolitis and propose CX3CR1 as a potential therapeutic target.

Our results indicate an association between a common genotype with severe RSV infection. This observation supports the previously reported results indicating RANTES as an important mediator of RSV infection.

Respiratory syncytial virus (RSV)-induced lower respiratory tract disease is a common problem in children and adults in Western societies. The clinical range of RSV infection from asymptomatic to respiratory distress syndrome is believed to be the outcome of viral and host immunity interactions. Genes associated with immune response are of particular interest regarding genetic predisposition to severe RSV infection. Several investigators have sought to identify genetic markers for high-risk patients, and more than 20 independent studies in the medical literature assess the impact of genetic variations-mostly single nucleotide polymorphisms-on the clinical presentation of RSV-induced disease. Several candidate gene loci have been tested in association studies based on the concept that a particular allele is a significant risk factor for a phenotype of interest. Despite the wealth of information available, we are still far from evolving a practical and cost-effective screening tool; certain flaws in association studies first need to be overcome. The development of haplotype-based analysis for candidate loci across the genome, along with advances in biostatistics and bioinformatics, would facilitate the assessment of the relative contribution of genetic markers to disease susceptibility in RSV infection.

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