OBJECTIVES : Rotavirus causes gastroenteritis in children. The introduction of vaccines protecting children against some rotavirus serotypes induced a redistribution of circulating serotypes in children. The mechanisms driving this redistribution are not well understood. One hypothesis is that remaining unvaccinated children are more exposed to adults who have a different serotype distribution. The presented model tests the plausibility of this hypothesis.

METHODS : A transmission model was developed with two serotypes circulating in children and adults. Transmission was considered within each population and from adults to children. The model assumed closed populations but with different children and adult serotype distributions prior to vaccination. Vaccination protecting children against both serotypes was introduced, after which the model estimated shifts in the new postvaccine serotype distribution equilibrium. Default parameters were identified, and scenario analyses were tested on vaccine coverage rate, levels of adult-to-child transmission rates, and relative population sizes.

RESULTS : The distributions between the two serotypes prior to vaccination were 25%:75% in children and 50%:50% in adults, and the proportions infected were 43% and 33%, respectively. For the default parameters, 80% vaccine coverage reduced the proportion of children infected by 92% and shifted the child serotype distribution at equilibrium toward the adult distribution to 47%:53%. Similar results were observed for all parameter scenarios, with the serotype distribution among infected children shifting closer to the adult distribution as vaccine coverage increased.

CONCLUSIONS : The model demonstrates that serotype distribution in children after vaccination may be influenced by the adult serotype distribution, with higher vaccine coverage shifting the child distribution closer to the adult distribution. As adult-to-child infection becomes more common than child-to-child infection, the adult serotype distribution becomes more prominent in the child population. These results support the hypothesis that rotavirus exposure from adult populations contributes to observed shifts in rotavirus serotype distributions in children after vaccine introduction.