Measurement of antibody against contemporary virus lineages of human respiratory syncytial virus sub-group A in infants and their mothers.
BACKGROUND
Human respiratory syncytial virus (hRSV) infects the majority of infants in their first year of life. Maternal antibodies offer some protection although a small proportion of infected infants develop bronchiolitis and require admission to hospital. A number of lineages of the virus co-circulate in the population and the prevalent virus lineage changes from epidemic to epidemic. The effect of antigenic variation between virus lineages upon the protection offered by maternal antibodies has not been assessed.


OBJECTIVE
To explore the possibility that infants may develop bronchiolitis because of a virus lineage-specific deficiency in their maternal antibodies.


METHODS
Virus isolates from infants admitted to hospital in Newcastle upon Tyne with hRSV infection during two consecutive winter epidemics were classified into lineages by genotypic analysis. Antibodies to the surface glycoproteins of contemporary sub-group A lineages and to the A2 virus strain were assayed in the acute sera of infected infants, in a group of uninfected infants and in the mothers of both groups.


RESULTS
Four lineages of sub-group A hRSV were found circulating during the study period. Antibody titres measured against all virus lineages in the acute serum of infants with hRSV bronchiolitis were similar. In the uninfected infants and in the mothers of both infected and uninfected groups antibody titres to all four contemporary virus lineages were also similar. However, in these groups antibodies to the A2 virus strain were four-fold lower than those to contemporary isolates.


CONCLUSIONS
Infants admitted to hospital with hRSV bronchiolitis exhibited no apparent selective deficiency in maternal antibodies to the viral glycoproteins of the infecting virus strain or lineage.
McGill
A
A
Department of Microbiology and Immunology, The Medical School, The University of Newcastle Upon Tyne, Framlington Place, Newcastle Upon Tyne NE2 4HH, UK.
Greensill
J
J
Craft
A W
AW
Fenwick
F
F
Toms
G L
GL
D000914:Antibodies, Viral / Q000097:blood*; D000940:Antigenic Variation; D000956:Antigens, Viral / Q000276:immunology; D001988:Bronchiolitis / Q000276:immunology / Q000821:virology; D016172:DNA Fingerprinting; D018076:DNA, Complementary; D005260:Female; D005838:Genotype; D006801:Humans; D007112:Immunity, Maternally-Acquired; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007223:Infant; D010802:Phylogeny; D012150:Polymorphism, Restriction Fragment Length; D012367:RNA, Viral / Q000302:isolation & purification; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology* / Q000821:virology*; D018113:Respiratory Syncytial Virus, Human / Q000145:classification / Q000235:genetics / Q000276:immunology* / Q000302:isolation & purification; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017422:Sequence Analysis, DNA; D006113:United Kingdom / Q000453:epidemiology; D014764:Viral Proteins / Q000235:genetics
D000914:Antibodies, Viral; D000956:Antigens, Viral; D018076:DNA, Complementary; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D012367:RNA, Viral; D014764:Viral Proteins