The effect of SARS-CoV-2 vaccination on post-acute COVID-19 syndrome (PASC): A prospective cohort study 8 245 3 months following matched time-point, whichever occurred first. Participants were allowed to contribute multiple periods of unvaccinated follow-up and could contribute to both vaccinated and unvaccinated time intervals, provided that symptom data were available for at least one follow-up time-point after the matched time-point. In order to ensure that symptom data were measured from the same baseline for each participant, we divided follow-up in monthly intervals since illness onset according to the date on which surveys were completed. We modelled the mean total number of symptoms at each time-point using linear regression, which was compared between the matched vaccinated and unvaccinated individuals using Wald χ2 tests. We bootstrapped variance estimates to ensure that variance was independent and identically distributed across participants. These variance estimates were used to calculate 95% confidence intervals (CIs) around the mean number of PASC symptoms at each time-point. Secondly, we used exact logistic regression to compare the odds of having recovered fully from PASC by the end of matched follow-up intervals between matched pairs of vaccinated and unvaccinated individuals. We then explored the association between early antibody titers and consequent development of PASC. Among participants with at least 3 months of follow-up after illness onset, we used a Bayesian multilevel model to compare IgG antibody neutralising and binding titers (to WT-D614G spike [S] and receptor binding domain [RBD]) measured 3060 days after illness onset between those who did and did not develop PASC. This model estimates the absolute difference in means between groups, while pooling estimates across study participants. Differences in posterior means were mean-centred such that effect sizes shown could be compared on a common scale. To assess the effect of COVID-19 severity, the analysis was repeated, this time stratifying by clinical severity group. To assess the association between antibody kinetics and PASC status, we stratified individuals with and without PASC at 3 months after illness onset and fitted patients with at least two datapoints where spike/RBD-binding IgG measurements were made to a constant decay model. We performed Bayesian hierarchical linear regression of the log response variable (Y) against time since symptom onset (t), partially pooling decay rates across participants (i): Y=βi t + ci where βi and ci are the participant-specific decay rate and intercept.
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