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Competition between RSV and influenza: Limits of modelling inference from surveillance data

Respiratory Syncytial Virus (RSV) and Influenza cause a large burden of disease. Evidence of their interaction via temporary cross-protection implies that prevention of one could inadvertently lead to an increase in the burden of the other. However, evidence for the public health impact of such inte...

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Detalles Bibliográficos
Autores principales: Waterlow, Naomi R., Flasche, Stefan, Minter, Amanda, Eggo, Rosalind M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8193815/
https://www.ncbi.nlm.nih.gov/pubmed/33838587
http://dx.doi.org/10.1016/j.epidem.2021.100460
Descripción
Sumario:Respiratory Syncytial Virus (RSV) and Influenza cause a large burden of disease. Evidence of their interaction via temporary cross-protection implies that prevention of one could inadvertently lead to an increase in the burden of the other. However, evidence for the public health impact of such interaction is sparse and largely derives from ecological analyses of peak shifts in surveillance data. To test the robustness of estimates of interaction parameters between RSV and Influenza from surveillance data we conducted a simulation and back-inference study. We developed a two-pathogen interaction model, parameterised to simulate RSV and Influenza epidemiology in the UK. Using the infection model in combination with a surveillance-like stochastic observation process we generated a range of possible RSV and Influenza trajectories and then used Markov Chain Monte Carlo (MCMC) methods to back-infer parameters including those describing competition. We find that in most scenarios both the strength and duration of RSV and Influenza interaction could be estimated from the simulated surveillance data reasonably well. However, the robustness of inference declined towards the extremes of the plausible parameter ranges, with misleading results. It was for instance not possible to tell the difference between low/moderate interaction and no interaction. In conclusion, our results illustrate that in a plausible parameter range, the strength of RSV and Influenza interaction can be estimated from a single season of high-quality surveillance data but also highlights the importance to test parameter identifiability a priori in such situations.