Was R < 1 before the English lockdowns? On modelling mechanistic detail, causality and inference about Covid-19

Detail is a double edged sword in epidemiological modelling. The inclusion of mechanistic detail in models of highly complex systems has the potential to increase realism, but it also increases the number of modelling assumptions, which become harder to check as their possible interactions multiply. In a major study of the Covid-19 epidemic in England, Knock et al. (2020) fit an age structured SEIR model with added health service compartments to data on deaths, hospitalization and test results from Covid-19 in seven English regions for the period March to December 2020. The simplest version of the model has 684 states per region. One main conclusion is that only full lockdowns brought the pathogen reproduction number, R, below one, with R ≫ 1 in all regions on the eve of March 2020 lockdown. We critically evaluate the Knock et al. epidemiological model, and the semi-causal conclusions made using it, based on an independent reimplementation of the model designed to allow relaxation of some of its strong assumptions. In particular, Knock et al. model the effect on transmission of both non-pharmaceutical interventions and other effects, such as weather, using a piecewise linear function, b(t), with 12 breakpoints at selected government announcement or intervention dates. We replace this representation by a smoothing spline with time varying smoothness, thereby allowing the form of b(t) to be substantially more data driven, and we check that the corresponding smoothness assumption is not driving our results. We also reset the mean incubation time and time from first symptoms to hospitalisation, used in the model, to values implied by the papers cited by Knock et al. as the source of these quantities. We conclude that there is no sound basis for using the Knock et al. model and their analysis to make counterfactual statements about the number of deaths that would have occurred with different lockdown timings. However, if fits of this epidemiological model structure are viewed as a reasonable basis for inference about the time course of incidence and R, then without very strong modelling assumptions, the pathogen reproduction number was probably below one, and incidence in substantial decline, some days before either of the first two English national lockdowns. This result coincides with that obtained by more direct attempts to reconstruct incidence. Of course it does not imply that lockdowns had no effect, but it does suggest that other non-pharmaceutical interventions (NPIs) may have been much more effective than Knock et al. imply, and that full lockdowns were probably not the cause of R dropping below one.