Metadata about: Containing the recent West African outbreak of Ebola virus (EBOV) required the deployment of substantial global resources. Despite recent progress in analysing and modelling EBOV epidemiological data, a complete characterization of the spatio-temporal spread of Ebola cases remains a challenge. In this work, we offer a novel perspective on the EBOV epidemic in Sierra Leone that uses individual virus genome sequences to inform population-level, spatial models. Calibrated to phylogenetic linkages of virus genomes, these spatial models provide unique insight into the disease mobility of EBOV in Sierra Leone without the need for human mobility data. Consistent with other investigations, our results show that the spread of EBOV during the beginning and middle portions of the epidemic strongly depended on the size of and distance between populations. Our phylodynamic analysis also revealed a change in model preference towards a spatial model with power-law characteristics in the latter portion of the epidemic, correlated with the timing of major intervention campaigns. More generally, we believe this framework, pairing molecular diagnostics with a dynamic model selection procedure, has the potential to be a powerful forecasting tool along with offering operationally relevant guidance for surveillance and sampling strategies during an epidemic.

About: Containing the recent West African outbreak of Ebola virus (EBOV) required the deployment of substantial global resources. Despite recent progress in analysing and modelling EBOV epidemiological data, a complete characterization of the spatio-temporal spread of Ebola cases remains a challenge. In this work, we offer a novel perspective on the EBOV epidemic in Sierra Leone that uses individual virus genome sequences to inform population-level, spatial models. Calibrated to phylogenetic linkages of virus genomes, these spatial models provide unique insight into the disease mobility of EBOV in Sierra Leone without the need for human mobility data. Consistent with other investigations, our results show that the spread of EBOV during the beginning and middle portions of the epidemic strongly depended on the size of and distance between populations. Our phylodynamic analysis also revealed a change in model preference towards a spatial model with power-law characteristics in the latter portion of the epidemic, correlated with the timing of major intervention campaigns. More generally, we believe this framework, pairing molecular diagnostics with a dynamic model selection procedure, has the potential to be a powerful forecasting tool along with offering operationally relevant guidance for surveillance and sampling strategies during an epidemic.

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