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Chapter 13 : Prevention of Respiratory Syncytial Virus Infection: From Vaccine to Antibody

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Abstract:

Respiratory syncytial virus (RSV) poses a serious and significant health problem. RSV was discovered in 1956 and quickly became recognized as the leading cause of lower respiratory tract disease in infants and young children ( ). Preterm infants and young children with bronchopulmonary dysplasia (BPD) or congenital heart disease (CHD) are at high risk of serious RSV infection and may require hospitalizations and stays in the pediatric intensive care unit ( ). Although these high-risk groups experience an increased incidence of RSV disease, it is important to note that the majority of infants hospitalized for RSV are previously healthy, nonpremature children ( ). In children less than 5 years of age, RSV infections account for 50 to 80% of winter bronchiolitis hospitalizations and 30 to 60% of pneumonia hospitalizations ( ). RSV bronchiolitis is reported as the leading cause of hospitalization for infants less than 12 months of age ( ). Hospitalization for RSV can reach rates of 1 to 20 per 1,000 infants less than 1 year of age in developed countries ( ). Although not common, RSV can be fatal, as 140 to 500 infant deaths are attributed to RSV each year in the United States ( ). In addition to infants and young children, another risk group for RSV disease is the elderly. In fact, while mortality in children due to RSV disease has decreased over the years, mortality due to RSV disease among the elderly is still a significant problem ( ). Also, immunosuppressed leukemia patients or patients receiving stem cell transplant therapy experience as much as 80 to 100% mortality upon RSV infection and are therefore a high-risk group for RSV disease ( ).

Citation: Huang K, Wu H. 2015. Prevention of Respiratory Syncytial Virus Infection: From Vaccine to Antibody, p 221-236. In Crowe J, Boraschi D, Rappuoli R (ed), Antibodies for Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.AID-0014-2014

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Lower Respiratory Tract Infections
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Figures

Image of Figure 1
Figure 1

The illustration depicts the mechanism of action of RSV-neutralizing mAbs, palivizumab and motavizumab. An RSV virion is illustrated at the top left corner showing that the F and G proteins are located on the surface of the virion and the drawing below depicts G-protein-mediated attachment to cells followed by F protein mediated virus-cell fusion. The steps of fusion are shown on the top right. F protein also mediates cell-to-cell fusion resulting in syncytium formation, depicted in the middle drawing. In the final drawing on the bottom, an RSV-neutralizing antibody, either palivizumab or motavizumab, binds to F protein and blocks virus replication. It was determined that palivizumab and motavizumab do not inhibit RSV attachment, but rather F-protein-mediated virus-cell fusion and syncytia formation as reported recently ( ). doi:10.1128/microbiolspec.AID-0014-2014.f1

Citation: Huang K, Wu H. 2015. Prevention of Respiratory Syncytial Virus Infection: From Vaccine to Antibody, p 221-236. In Crowe J, Boraschi D, Rappuoli R (ed), Antibodies for Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.AID-0014-2014
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Image of Figure 2a
Figure 2a

(A) Palivizumab was generated by CDR-grafting humanization of murine mAb 1129. Murine CDR regions are depicted in ball structure. The remaining regions are human origin. (B) Top view of the six murine CDRs that were grafted to human frameworks. doi:10.1128/microbiolspec.AID-0014-2014.f2

Citation: Huang K, Wu H. 2015. Prevention of Respiratory Syncytial Virus Infection: From Vaccine to Antibody, p 221-236. In Crowe J, Boraschi D, Rappuoli R (ed), Antibodies for Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.AID-0014-2014
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Download as Powerpoint
Image of Figure 2b
Figure 2b

(A) Palivizumab was generated by CDR-grafting humanization of murine mAb 1129. Murine CDR regions are depicted in ball structure. The remaining regions are human origin. (B) Top view of the six murine CDRs that were grafted to human frameworks. doi:10.1128/microbiolspec.AID-0014-2014.f2

Citation: Huang K, Wu H. 2015. Prevention of Respiratory Syncytial Virus Infection: From Vaccine to Antibody, p 221-236. In Crowe J, Boraschi D, Rappuoli R (ed), Antibodies for Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.AID-0014-2014
Permissions and Reprints Request Permissions
Download as Powerpoint

References

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