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Antiviral Immune Responses and Lung Inflammation after Respiratory Syncytial Virus Infection

Department of Respiratory Medicine, National Heart and Lung Institute, Faculty of Medicine, Imperial College, London, United Kingdom

Correspondence and requests for reprints should be addressed to Peter J. M. Openshaw, M.D., Ph.D., Department of Respiratory Medicine, National Heart and Lung and Wright Fleming Institutes, Faculty of Medicine, Imperial College London, Paddington, London W2 1PG, UK. E-mail: p.openshaw{at}imperial.ac.uk

Respiratory syncytial virus (RSV) is one of the commonest and most troublesome viruses of infancy. It causes most cases of bronchiolitis, which is associated with wheezing in later childhood. In primary infection, the peak of disease coincides not with the peak of viral replication but with the development of specific T and B cell responses. This immune response is apparently responsible for much of the disease. Animal models clearly show that a range of immune responses can enhance disease severity, particularly after vaccination with formalin-inactivated RSV. Prior immune sensitization leads to exuberant chemokine production, an excessive cellular influx, and an overabundance of cytokines during RSV challenge. The inflammatory host response to viral infection may be relevant not only to childhood bronchiolitis, but also to obstructive lung diseases in adults.

Key Words: animal models • asthma • bronchiolitis • viral disease