Speaker
Description
Enterovirus D68 (EV-D68), first discovered in the 1960s, emerged to cause outbreaks of severe respiratory disease and polio-like paralysis in 2014. The transmission dynamics of EV-D68 before its emergence are poorly understood due to its clinical similarities to other respiratory infections. These similarities also complicate detection without specific testing. Despite this, extensive genetic sequence data is available for EV-D68, driven by widespread recent sampling in the US and Europe. This data primarily covers the VP1 capsid protein used for viral typing and clade determination, but full-length genomes are also increasingly regularly sequenced and published. Older genetic sequence data are also publicly available, dating back to the 1990s. Here we aim to reconstruct the effective reproduction number (Rt) of two EV-D68 superclades over time in Northern America and Western Europe using a multitype birth-death phylodynamic model (BDMM prime). The model allows for changes in Rt at two time points each year (aligned with known EV-D68 seasonality), as well as an overall change in sampling intensity in 2014, at the time of the first major reported outbreak. The model also includes migration between Northern America and Western Europe.
Using reconstructed EV-D68 incidence, we find a strong association between the B+C clade and reported paralysis cases, which we do not find for the A+D clade. We also find that the B+C clade was 2.2 times more likely to be sampled than the A+D clade. Overall, these results suggest more severe outcomes are associated with clade B+C infections, thus making detection of this clade more likely.
This study demonstrates how viral diversity can be used to infer viral spread, allowing us to reconstruct key epidemiological parameters for EV-D68 in the absence of reliable incidence data.
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