Respiratory syncytial virus disease mechanisms implicated by human, animal model, and in vitro data facilitate vaccine strategies and new therapeutics

被引:42
作者
Moore, Martin L. [1 ]
Peebles, R. Stokes, Jr. [1 ]
机构
[1] Vanderbilt Univ, Sch Med, Dept Med, Div Allergy Pulm & Crit Care Med, Nashville, TN 37232 USA
关键词
respiratory syncytial virus; immunopathology; interferon; T cells; cytokines; chemokines;
D O I
10.1016/j.pharmthera.2006.04.008
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis, pneumonia, mechanical ventilation, and respiratory failure in infants in the US. No effective post-infection treatments are widely available, and currently there is no vaccine. RSV disease is the result of virus-induced airway damage and complex inflammatory processes. The outcome of infection depends on host and viral genetics. Here, we review disease mechanisms in primary RSV infection that are implicated by clinical studies, in vitro systems, and animal models. Defining RSV disease mechanisms is difficult because there is a wide range of RSV disease phenotypes in humans, and there are disparities in RSV disease phenotypes among the animal models of RSV infection. However, host factors identified by multiple lines of investigation as playing important roles in RSV pathogenesis are providing key insights. A better understanding of RSV molecular biology and RSV pathogenesis is facilitating rational vaccine design strategies and molecular targets for new therapeutics. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:405 / 424
页数:20
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