Journal
VIRAL IMMUNOLOGY
Volume 17, Issue 3, Pages 370-380Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/vim.2004.17.370
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Funding
- NIAID NIH HHS [R01-AI47226] Funding Source: Medline
- NIDCD NIH HHS [R01-DC06468] Funding Source: Medline
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Respiratory syncytial virus (RSV), a member of the Paramyxoviridae family, is a major clinical problem causing yearly epidemics of severe lower airway disease in both infants and the elderly. Attempts at vaccination have been frustrated by both the poor immunogenicity of this virus, and the severe immunopathology observed in early vaccine trials. Primary infection generally occurs in infancy, with approximately 5% of infected infants requiring hospitalization. Equally problematic is the apparent link between severe RSV disease and the later development of allergy and asthma. While there is no evidence that natural infection promotes Th2 predominance, development of enhanced eosinophilic disease in children receiving inactivated virus administered with a commonly used adjuvant demonstrated how easily the balance between immune-mediated protection and immune-mediated pathology can be perturbed. In this review we have focused on studies carried out in the mouse model aimed at determining the correlates of RSV protection and explaining the mechanism of vaccine enhanced immunopathology.
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