Abstract

Background. Respiratory syncytial virus (RSV) vaccine development for direct protection of young infants faces substantial obstacles. Assessing the potential of indirect protection using different strategies, such as targeting older children or mothers, requires knowledge of the source of infection to the infants.Methods. We undertook a prospective study in rural Kenya. Households with a child born after the preceding RSV epidemic and ≥1 elder sibling were recruited. Nasopharyngeal swab samples were collected every 3–4 days irrespective of symptoms from all household members throughout the RSV season of 2009–2010 and tested for RSV using molecular techniques.Results. From 451 participants in 44 households a total of 15 396 nasopharyngeal swab samples were samples were collected, representing 86% of planned sampling. RSV was detected in 37 households (84%) and 173 participants (38%) and 28 study infants (64%). The infants acquired infection from within (15 infants; 54%) or outside (9 infants; 32%) the household; in 4 households the source of infant infection was inconclusive. Older children were index case patients for 11 (73%) of the within-household infant infections, and 10 of these 11 children were attending school.Conclusion. We demonstrate that school-going siblings frequently introduce RSV into households, leading to infection in infants.

Highlights

  • Respiratory syncytial virus (RSV) vaccine development for direct protection of young infants faces substantial obstacles

  • RSV was detected in 37 households (84%) and 173 participants (38%) and 28 study infants (64%)

  • We demonstrate that school-going siblings frequently introduce RSV into households, leading to infection in infants

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Summary

Methods

We undertook a prospective study in rural Kenya. Households with a child born after the preceding RSV epidemic and ≥1 elder sibling were recruited. Nasopharyngeal swab samples were collected every 3–4 days irrespective of symptoms from all household members throughout the RSV season of 2009–2010 and tested for RSV using molecular techniques. Study Area The study was undertaken in rural coastal Kenya within the Kilifi Health and Demographic Surveillance System (KHDSS) [18]. The long ectodomain region of the RSV attachment (G) gene was sequenced as described elsewhere [22]. Comparison of the primary-infant case pairs involved regions 648 and 732 nucleotides long for RSV groups A and B, respectively. 1 RSVpositive specimen (with the lowest cycle threshold values) was selected from each pair for sequencing. Random sequences (10 for each RSV group, collected from children admitted at the Kilifi District Hospital during a similar period) were included in the trees as references

Results
Discussion
Conclusion

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