Antibody response and avidity of respiratory syncytial virus-specific total IgG, IgG1, and IgG3 in young children

✍ Scribed by G.R.O. Freitas; D.A.O. Silva; J. Yokosawa; N.T. Paula; L.F. Costa; B.M. Carneiro; L.Z.G. Ribeiro; T.F.M. Oliveira; J.R. Mineo; D.A.O. Queiróz

• Publisher: John Wiley and Sons
• Year: 2011
• Tongue: English
• Weight: 165 KB
• Volume: 83
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.22134

✦ Synopsis

Abstract

Respiratory syncytial virus (RSV) is a major cause of acute respiratory disease in infants and young children. Considering that several aspects of the humoral immune response to RSV infection remain unclear, this study aimed to investigate the occurrence, levels, and avidity of total IgG, IgG1, and IgG3 antibodies against RSV in serum samples from children ≤5 years old. In addition, a possible association between antibody avidity and severity of illness was examined. The occurrence and levels of RSV‐specific IgG depended on age, with infants <3 months old displaying high levels of antibodies, which were probably acquired from the mother. Children ≥24 months old also showed frequent occurrence and high levels of IgG, which was produced actively during infection. In addition, the avidity assay showed that the avidity of RSV‐specific total IgG and IgG1 was lower in infants <3 months old who had acute respiratory disease than in age‐matched controls. The avidity of RSV‐specific IgG detected in children ≥24 months old with lower respiratory infection was lower than that in children with upper respiratory infection. These results indicate that the presence of high avidity RSV‐specific IgG antibodies may lead to better protection against RSV infection in children <3 months old, who may have a lower probability of developing disease of increased severity. In addition, children ≥24 months old with RSV‐specific IgG antibodies of low avidity tended to develop more severe RSV illness. These findings may be helpful in establishing vaccination schedules when a vaccine becomes available. J. Med. Virol. 83:1826–1833, 2011. © 2011 Wiley‐Liss, Inc.