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Influence of Respiratory Syncytial Virus Strain Differences on Pathogenesis and Immunity

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Challenges and Opportunities for Respiratory Syncytial Virus Vaccines

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 372))

Abstract

Molecular epidemiology studies have provided convincing evidence of antigenic and sequence variability among respiratory syncytial virus (RSV) isolates. Circulating viruses have been classified into two antigenic groups (A and B) that correlate with well-delineated genetic groups. Most sequence and antigenic differences (both inter- and intra-groups) accumulate in two hypervariable segments of the G-protein gene. Sequences of the G gene have been used for phylogenetic analyses. These studies have shown a worldwide distribution of RSV strains with both local and global replacement of dominant viruses with time. Although data are still limited, there is evidence that strain variation may contribute to differences in pathogenicity. In addition, there is some but limited evidence that RSV variation may be, at least partially, immune (antibody) driven. However, there is the paradox in RSV that, in contrast to other viruses (e.g., influenza viruses) the epitopes recognized by the most effective RSV-neutralizing antibodies are highly conserved. In contrast, antibodies that recognize strain-specific epitopes are poorly neutralizing. It is likely that this apparent contradiction is due to the lack of a comprehensive knowledge of the duration and specificities of the human antibody response against RSV antigens. Since there are some data supporting a group- (or clade-) specific antibody response after a primary infection in humans, it may be wise to consider the incorporation of strains representative of groups A and B (or their antigens) in future RSV vaccine development.

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Acknowledgments

Work in the Madrid laboratory is currently funded by grants GR09/0039 from Instituto de Salud Carlos III and SAF2009-11632 and SAF2012-31217 from Plan Nacional de I+D+i. Work in the Atlanta laboratory is supported by the following grants: NIH 1R01AI087798 and NIH 1U19AI095227.

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Authors and Affiliations

  1. Unidad de Biología Viral, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Madrid, Spain

    José A. Melero

  2. Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III, Madrid, Spain

    José A. Melero

  3. Department of Pediatrics, Emory University, Atlanta, GA, USA

    Martin L. Moore

  4. Children’s Healthcare of Atlanta, Atlanta, GA, USA

    Martin L. Moore

Authors
  1. José A. Melero
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  2. Martin L. Moore
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Correspondence to José A. Melero .

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Editors and Affiliations

  1. Department of Pediatrics and Children's Healthcare of Atlanta, Emory University, Atlanta, Georgia, USA

    Larry J. Anderson

  2. Vaccine Research Center, NIH Natl. Inst. of Allergy & Infect. Dis., Bethesda, Maryland, USA

    Barney S. Graham

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Melero, J.A., Moore, M.L. (2013). Influence of Respiratory Syncytial Virus Strain Differences on Pathogenesis and Immunity. In: Anderson, L., Graham, B. (eds) Challenges and Opportunities for Respiratory Syncytial Virus Vaccines. Current Topics in Microbiology and Immunology, vol 372. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-38919-1_3

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