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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.
Peter Openshaw (1995) studied this question.