Antibody response after RSV infection in children younger than 1 year of age living in a rural area of Mozambique

Abstract

Serological responses have been studied in respiratory syncytial virus (RSV) infected children < 1 year of age attending the outpatient department of the Manhiça District Hospital (Mozambique). Molecular characterization of viral RNA in nasopharyngeal aspirates from the infected children indicated a high level of genetic uniformity among the infecting viruses, all of which belonged to a single genotype of RSV group A. A representative virus strain, Moz00, was isolated from one of the infants and was used, together with the group A strain A2 and the group B strain 8/60, as antigens in the quantification of infant antibody responses. In this study, 97.5% (39/40) and 96.4% (27/28) of infected children produced an antibody response against Moz00 detected by the membrane fluorescent antibody test (MFAT) and the neutralization test (NT), respectively. Seroconversion rates decreased when the A2 and 8/60 strains were used as antigen in MFAT (95.4% and 88.2%, respectively) or NT (81.8% and 54.5%, respectively), indicating that antibody responses had both group- and strain-specific components. Antibodies in convalescent sera of infected children were compared with maternally derived antibodies detected in a group of children also < 1 year of age, but with no evidence of RSV infection. The convalescent sera exhibited reduced neutralizing capacity when the 8/60 strain was used as antigen (P = 0.028), suggesting that the infant antibody response lacks neutralizing capacity against strains of the heterologous virus group. Restricted cross-reactivity and neutralizing capacity of antibodies generated by young children might be expected to induce only moderate protection in subsequent epidemics against genetically distant strains.

Antibody response to respiratory syncytial virus infection in children <18 months old

“…19 In this study, viral type, viral load, and duration of shedding did not influence the antibody response. The finding of a lack of a correlation between viral type and antibody response is in disagreement with the data reported by Roca et al 15 These authors found that although an immune response after RSV infection was evidenced in all children regardless of the viral type, different RSV strains could evoke different immune responses in patients infected by RSV A, who showed the highest increments in antibody titres. In our study population, no statistically significant difference in GMT was found between children infected by RSV type A and those affected by RSV type B, although GMT fold changes were higher in RSV-A cases.…”

“…On the other hand, all the other studies regarding specific antibody production in children infected by RSV showed results quite similar to those reported in our study. [10][11][12][13][14][15][16] Moreover, similar results were recently confirmed by Sande et al, 18 who reported that in comparison to the mean acute phase antibody titer, the mean convalescent titer was lower in the 0-1.9 month age class, no different in the 2-3.9 month age class and greater in all age classes 4 months.…”

“…To evaluate immune response according to age, the cut-off level of 7 months was chosen according to previous studies showing that the greatest immune response to RSV infection occurs after this age. [9][10][11][12][13][14][15] Those <7 months old had higher baseline levels than those 7 months old. However, older children showed a significantly higher increase in the antibody response from V1 to V2 in comparison to those aged <7 months (p<0.001).…”

The human neonatal B cell response to respiratory syncytial virus uses a biased antibody variable gene repertoire that lacks somatic mutations

“…One infant in this study who was experiencing a second documented RSV infection within the first few months of life still lacked mutations in RSV-specific gene segments. These data strongly suggest that inefficiencies in the molecular and cellular mechanisms controlling somatic hypermutation may underlie poor infant antibody responses to vaccines and viral infections (Brandenburg et al, 1997; Murphy et al, 1986a; Murphy et al, 1986b; Roca et al, 2003). Zemlin et al analyzed global Ig repertoire and discovered that preterm infants exhibited reduced somatic mutations compared with term infants (Zemlin et al, 2007).…”

“…Numerous studies have documented the poor humoral immune response of infants to respiratory syncytial virus (RSV) and other pathogens that commonly cause infection early in life (Brandenburg et al, 1997; Murphy et al, 1986a; Murphy et al, 1986b; Roca et al, 2003). Passively-acquired maternal antibodies suppress the primary antibody response in infants.…”