Host immunity during RSV pathogenesis.
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.
Bueno
Susan M
SM
Millennium Nucleus on Immunology and Immunotherapy. Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Chile.
González
Pablo A
PA
Pacheco
Rodrigo
R
Leiva
Eduardo D
ED
Cautivo
Kelly M
KM
Tobar
Hugo E
HE
Mora
Jorge E
JE
Prado
Carolina E
CE
Zúñiga
Juan P
JP
Jiménez
Jorge
J
Riedel
Claudia A
CA
Kalergis
Alexis M
AM
D000956:Antigens, Viral / Q000276:immunology; D003428:Cross Infection / Q000276:immunology* / Q000473:pathology; D003713:Dendritic Cells / Q000276:immunology; D006801:Humans; D007109:Immunity; D007114:Immunization; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology* / Q000473:pathology; D012136:Respiratory Syncytial Viruses / Q000472:pathogenicity*; D018418:Th2 Cells / Q000276:immunology; D038301:Virus Inactivation
D000956:Antigens, Viral