Passive and Acquired Immunity to Respiratory Syncytial Virus in Young Children in Rural Kenya

Ochola-Opiyo, Beldinah R. (2008). Passive and Acquired Immunity to Respiratory Syncytial Virus in Young Children in Rural Kenya. PhD thesis The Open University.



The rate of decay and the subsequent antibody responses to RSV are poorly defined in young infants and children who possess maternally derived respiratory syncytial virus (RSV) antibodies. A birth cohort from rural Kenya was studied intensively to monitor infections from whom blood samples were collected at regular intervals to describe the age-related serological characteristics. A simple linear regression model was used to calculate the rate of RSV-specific maternal antibody decline. In addition, the effect of risk factors on cord blood titres was investigated. Using the random effects model, the half-life of RSV maternal antibodies was calculated to be 79 days. Although 97% of infants were bom with RSV-specific maternal antibodies, it was noted that infants who went on to experience an infection in early life, had lower starting titres of RSV maternal antibodies in comparison to infants who did not have any clinically confirmed infection in the first 6 months. Additionally, clinically confirmed infections within the first 6 months of life had no effect on the rate of decay of maternal antibodies.

Both RSV group A and B were seen to circulate in the community in varying amounts, with RSV A seen to be the most dominant strain in the 4 epidemics experienced by the cohort. The same RSV strain was observed to cause both RSV-associated upper respiratory tract and lower respiratory tract infections. It was observed that there existed patterns of antibody decay and acquisition of RSV-specific immune responses that groups of children appeared to follow. A group of infants were seen to undergo clinical infection that was subsequently confirmed by the ELISA, or were observed to seroconvert in the absence of clinical symptoms, or infants did not experience any infection at all despite experiencing at least 2 epidemics. Post-infection dynamics showed classical boosting of RSV antibodies, which either quickly waned or remained elevated over time. Furthermore, the risk of re-infection with clinically identified RSV illness decreased with age, from an initial infection rate of 252 to 41/1000 child years observation.

In conclusion, the evidence shows that RSV maternal antibodies provide some protection against severe disease during the first 6-7 months. Since there is efficient transfer of antibodies from mother to child, maternal vaccination against RSV may be a useful strategy to consider. However, our observations show that these antibodies decline quickly, hence childhood vaccines should also be taken into consideration to augment the immune responses.

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