Titlebook: Challenges and Opportunities for Respiratory Syncytial Virus Vaccines; Larry J. Anderson,Barney S. Graham Book 2013 The Editor(s) (if appl

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Structure and Function of Respiratory Syncytial Virus Surface Glycoproteins (F), control the initial phases of infection. G targets the ciliated cells of the airways, and F causes the virion membrane to fuse with the target cell membrane. The F protein is the major target for antiviral drug development, and both G and F glycoproteins are the antigens targeted by neutralizi

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Respiratory Syncytial Virus and Reactive Airway Diseaseg, either by causing bronchiolitis or by inducing acute exacerbations of asthma. There has been a long-standing interest in whether severe RSV bronchiolitis in infancy is a risk factor for the development of asthma later in childhood. While epidemiologic studies have suggested that such a link exist

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Human Genetics and Respiratory Syncytial Virus Disease: Current Findings and Future Approachesvere bronchiolitis and pneumonia. Although there are several known risk factors for severe RSV disease, namely, premature birth, chronic lung disease, congenital heart disease, and T cell immunodeficiency, the majority of young children who develop severe RSV disease are otherwise healthy children.

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Respiratory Syncytial Virus Mechanisms to Interfere with Type 1 Interferonsection by these viruses triggers the innate antiviral response of the host, mainly type I interferon (IFN). Essentially all other viruses of this family produce IFN suppressor functions by co-transcriptional RNA editing. In contrast, RSV has evolved two unique nonstructural proteins, NS1 and NS2, to

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Host Gene Expression and Respiratory Syncytial Virus Infectioncell response screening that enable genome-wide analysis of cell factors involved in viral replication and disease. Application of both experimental and computational biology approaches have led to crucial insights into virus infection, its life cycle, and host gene targets for disease intervention.