Respiratory Syncytial Virus—Viral Biology and the Host Response

• Published in: The Journal of infection Vol. 45; no. 1; pp. 18 - 24
• Main Authors: Hacking, D., Hull, J.
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 01-07-2002; Elsevier
• Subjects: Biological and medical sciences; Epithelial Cells - immunology; Epithelial Cells - virology; Fundamental and applied biological sciences. Psychology; Genome, Viral; Humans; Microbiology; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains; Respiratory Syncytial Virus Infections - immunology; Respiratory Syncytial Virus Infections - virology; Respiratory Syncytial Viruses - genetics; Respiratory Syncytial Viruses - immunology; Respiratory Syncytial Viruses - physiology; Respiratory System - immunology; Respiratory System - virology; Virology; Human; Human respiratory syncytial virus; Immune response; Pneumovirinae; Respiratory epithelium; Chemical structure; Host virus relation; Paramyxoviridae; Virus; Pathogenicity; Mononegavirales; Epithelial cell; Pneumovirus; Genome
• ISSN: 0163-4453; 1532-2742
• DOI: 10.1053/jinf.2002.1015

Respiratory syncytial virus (RSV) is the most important cause of respiratory tract infection in infants. We have an incomplete understanding of the reasons why some infants are more severely affected by RSV than others. There is no effective antiviral treatment for the infection. Advances in our understanding of the biology of RSV, particularly in relation to the attachment protein G and the fusion protein F, have revealed potential targets for new antiviral therapies and vaccine development. In response to RSV infection an intense inflammatory response is triggered, mediated initially by the infected airway epithelial cells. Cell mediated responses are important in controlling the extent of infection and in viral clearance. Humoral responses are important in protection. There is early evidence that genetic variation of the host response can influence the outcome of RSV-induced bronchiolitis.