BMC Public Health (Oct 2024)
Model-based estimates of age-structured SARS-CoV-2 epidemiology in households
Abstract
Abstract Background Understanding how infectious disease transmission varies from person to person, including associations with age and contact behavior, can help design effective control strategies. Within households, transmission may be highly variable because of differing transmission risks by age, household size, and individual contagiousness. Our aim was to disentangle those factors by fitting mathematical models to SARS-CoV-2 household survey and serologic data. Methods We surveyed members of 3,381 Utah households from January-April 2021 and performed SARS-CoV-2 antibody testing on all available members. We paired these data with a probabilistic model of household importation and transmission composed of a novel combination of transmission variability and age- and size-structured heterogeneity. We calculated maximum likelihood estimates of mean and variability of household transmission probability between household members in different age groups and different household sizes, simultaneously with importation probability and probabilities of false negative and false positive test results. Results 12.8% of individual participants, residing in 17.4% of the participating households, showed serologic evidence of prior infection or reported a prior positive test on the survey. Serologically positive individuals in younger age groups were less likely than older adults to have tested positive during their infection according to our survey results. Our model results suggested that adolescents and young adults (ages 13–24) acquired SARS-CoV-2 infection outside the household at a rate substantially higher than younger children and older adults. Our estimate of the household secondary attack rate (HSAR) among adults aged 45 and older exceeded HSARs to and/or from younger age groups at a given household size. We found lower HSAR in households with more members, independent of age differences. The age-specific HSAR patterns we found could not be explained by age-dependent biological susceptibility and transmissibility alone, suggesting that age groups contacted each other at different rates within households. Conclusions We disentangled several factors contributing to age-specific infection risk, including non-household exposure, within-household exposure to specific age groups, and household size. Within-household contact rate differences played a significant role in driving household transmission epidemiology. These findings provide nuanced insights for understanding community outbreak patterns and mechanisms of differential infection risk.
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