Influence of respiratory syncytial virus strain differences on pathogenesis and immunity

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...

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Detalhes bibliográficos
Autores: Melero, Jose Antonio, Moore, Martin L
Formato: artículo
Fecha de publicación:2013
País:España
Recursos:Instituto de Salud Carlos III (ISCIII)
Repositorio:Repisalud
Idioma:inglés
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/8564
Acesso em linha:http://hdl.handle.net/20.500.12105/8564
Access Level:acceso abierto
Palavra-chave:Antibodies, Viral
Antibody Specificity
Antigenic Variation
Antigens, Viral
Evolution, Molecular
Humans
Molecular Epidemiology
Phylogeny
Respiratory Syncytial Virus Infections
Respiratory Syncytial Virus Vaccines
Respiratory Syncytial Virus, Human
Species Specificity
Vaccines, Subunit
Viral Fusion Proteins
Descrição
Resumo: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.