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Detection of human respiratory syncytial virus genotype specific antibody responses in infants
Author(s) -
McGill A.,
Greensill J.,
Marsh R.,
Craft A.W.,
Toms G.L.
Publication year - 2004
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20203
Subject(s) - virology , virus , antibody , biology , glycoprotein , genotype , heterologous , monoclonal antibody , antigen , population , immunology , gene , medicine , microbiology and biotechnology , genetics , environmental health
Infection and reinfection of infants with human respiratory syncytial virus (HRSV) occur despite the presence of serum anti‐viral glycoprotein antibodies similar to those, which afford protection in animal models of infection. Antigenic variation of the viral glycoproteins between different genotypes of the virus which co‐circulate in the population may contribute to the ability of the virus to escape from antibody‐mediated protection. In this study, we have investigated whether human infants infected with HRSV produced antibody responses recognising the antigenic differences between different contemporary genotypes of virus. Acute and convalescent sera from 26 infants were analysed for antibody responses to the glycoproteins of the virus isolated from their respiratory tract and to representative viruses of homologous and heterologous genotypes. All infants developed antibodies with similar reactivity for viruses of all contemporary isolates and genotypes when measured in an immunofluorescence assay against unfixed virus infected cells. However, when antibody responses to the individual glycoproteins were measured in a surace plasmon resonance (SPR) assay, although all infants developed genotype cross‐reactive antibodies to the F glycoprotein, anti‐G antibodies were detectable in only half of the infants and in all cases these were genotype specific. Possession of no or only genotype specific antibodies to the G glycoprotein may contribute to the susceptibility of infants to reinfection. In both assays, reactivity of anti‐glycoprotein antibodies with the sub‐group A archetypal strain, A2, was markedly lower than with any contemporary virus tested indicating that this strain alone is unsuitable for accurate assessment of infant antibody responses. J. Med. Virol. 74:492–498, 2004. © 2004 Wiley‐Liss, Inc.