Immunity and immunopathology to respiratory syncytial virus. The mouse model.
Infection with respiratory syncytial virus (RSV) is a major unsolved challenge for vaccine development. RSV is worldwide in distribution and infects almost all children during the first 2 yr of life. The mouse model of RSV lung disease has been very successful in reproducing many aspects of the human disease. In particular, the role of antiviral T cells in both eliminating virus and causing enhanced disease has been shown dramatically. This immunopathologic paradox is now more clearly understood than for any other common human infection, largely due to insights gained from the mouse model. This review focuses on the unique ability of different RSV proteins to prime for specific functional subsets in the mouse, and the association between sensitization to the major surface glycoprotein G, the induction of T helper 2 cells, and the subsequent appearance of lung eosinophilia during RSV infection.
Openshaw
P J
PJ
St. Mary's Hospital Medical School, Imperial College of Science, Technology and Medicine, London, United Kingdom.
D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology / Q000821:virology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology; D015707:HN Protein; D006801:Humans; D007114:Immunization; D051379:Mice; D008807:Mice, Inbred BALB C; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control; D012136:Respiratory Syncytial Viruses / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014759:Viral Envelope Proteins; D014764:Viral Proteins / Q000276:immunology
D015707:HN Protein; D014759:Viral Envelope Proteins; D014764:Viral Proteins; C116204:attachment protein G