Institutional members access full text with Ovid®

Share this article on:

Genetic Diversity of the Host and Severe Respiratory Syncytial Virus-Induced Lower Respiratory Tract Infection

Amanatidou, Virginia MD, PhD; Apostolakis, Stavros MD, PhD; Spandidos, Demetrios A. PhD, DSc

Pediatric Infectious Disease Journal: February 2009 - Volume 28 - Issue 2 - pp 135-140
doi: 10.1097/INF.0b013e31818c8d17
Review Article

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.

From the Department of Clinical Virology, University of Crete, Heraklion, Crete, Greece.

Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text; simply type the URL address into any Web browser to access this content. Clickable links to the material are provided in the HTML text and PDF of this article on the Journal's Web site (www.pidj.com).

Accepted for publication September 3, 2008.

Address for correspondence: Demetrios A. Spandidos, PhD, DSc, Department of Clinical Virology, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece. E-mail: spandidos@spandidos.gr.

© 2009 Lippincott Williams & Wilkins, Inc.