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Childhood infections
INTRODUCTION
Rubella is primarily a mild childhood disease, but acquiring the infection during the first 16 weeks of pregnancy is associated with the risk of fetal death or birth of a child with congenital rubella syndrome (CRS). CRS is a condition associated with a range of problems, from hearing impairment to brain damage. Estimates of the burden of CRS are high in many developing countries [1] and may frequently go unreported [2]. Since vaccination drives up the average age of infection, increasing the proportion of women of child-bearing age at risk [3-7], many countries in the developing world are not vaccinating against rubella [8], particularly given recent work indicating how partial vaccination of populations can increase the population-wide risk of CRS by allowing build-up of susceptible individuals in older age groups [9]. Multi-annual outbreak cycles are another factor that may allow such build-up because the deepened post-epidemic troughs may lead to local extinction and periods of lowered force of infection [10, 11].
Across much of the developing world, recent efforts to reduce the burden of measles mortality [12] via measles vaccination campaigns has lead to an increase in national vaccination coverage capacity and second-dose availability. In this context, it is of interest to revisit the risks associated with introduction of the rubella vaccine [13]. A major challenge to quantifying the potential CRS burden is that details of the drivers of rubella dynamics remain unclear. Where rubella dynamics have been described, multi-annual cycles of varying periodicity are generally observed [14] and competing explanatory mechanisms have been put forward (summarized in Table 1). Depending on the particular mechanism underlying multi-annual cycles, vaccination might either increase or decrease the period between major epidemics by shifting dynamics between multi-annual and annual regimens. Identifying both whether rubella dynamics are multi-annual, and if so, the mechanism underlying such multi-annual epidemics is therefore of programmatic interest. The mechanisms hypothesized hang on the treatment of seasonal patterns of transmission (Table 1), currently generally assumed to reflect term-time forcing, i.e. increases in transmission associated with aggregation of children in schools, and decreases during vacations [15]. However, whether this assumption is valid is unclear, since estimation of seasonal variation of transmission from time-series has been rare, and...