Host immunity during RSV pathogenesis

被引:79
作者
Bueno, Susan M. [1 ]
Gonzalez, Pablo A. [1 ]
Pacheco, Rodrigo [1 ]
Leiva, Eduardo D. [1 ]
Cautivo, Kelly M. [1 ]
Tobar, Hugo E. [1 ]
Mora, Jorge E. [1 ]
Prado, Carolina E. [1 ]
Zuniga, Juan P. [1 ]
Jimenez, Jorge [3 ]
Riedel, Claudia A. [4 ]
Kalergis, Alexis M. [1 ,2 ]
机构
[1] Pontificia Univ Catolica Chile, Fac Ciencias Biol, Dept Mol Genet & Microbiol, Millennium Nucleus Immunol & Immunotherapy, E-8331010 Santiago, Chile
[2] Pontificia Univ Catolica Chile, Dept Reumatol, Santiago, Chile
[3] Pontificia Univ Catolica Chile, Salud Publ, Santiago, Chile
[4] Univ Nacl Andres Bello, Santiago, Chile
关键词
respiratory syncytial virus; immune response; immunopathology; Th-2 immune response; T cells; dendritic cells;
D O I
10.1016/j.intimp.2008.03.012
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Infection by respiratory syncytial virus (RSV) is the leading cause of childhood hospitalization as well as a major health and economic burden worldwide. Unfortunately, RSV infection provides only limited immune protection to reinfection, mostly due to inadequate immunological memory, which leads to an exacerbated inflammatory response in the respiratory tract promoting airway damage during virus clearance. This exacerbated and inefficient immune-inflammatory response triggered by RSV, has often been attributed to the induction of a Th2-biased immunity specific for some of the RSV antigens. These features of RSV infection suggest that the virus might possess molecular mechanisms to enhance allergic-type immunity in the host in order to prevent clearance by cytotoxic T cells and ensure survival and dissemination to other hosts. In this review, we discuss recent findings that contribute to explain the components of the innate and adaptive immune response that are involved in RSV-mediated disease exacerbation. Further, the virulence mechanisms used by RSV to avoid activation of protective immune responses are described. (c) 2008 Elsevier B.V. All rights reserved.
引用
收藏
页码:1320 / 1329
页数:10
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