Speaker
Description
Approximately 90% of clinical diagnoses of influenza-like illness are not caused by influenza viruses (United States CDC), but rather by other respiratory pathogens, including respiratory syncytial virus (RSV). In temperate regions, including the United States, RSV demonstrates seasonality, with cases peaking in the colder months and approaching zero in the warmer months (Moriyama et al. 2020; Adams et al. 2023). The evolution of influenza viruses, including their patterns of global circulation (e.g., local persistence versus importation of variants across successive seasons) has been well characterized (Bedford et al. 2010; Bedford et al. 2015). However, it remains unknown how RSV circulates globally and locally over time.
There are multiple hypotheses regarding the source of pathogens that seed annual epidemics in temperate regions: (i) the tropics, (ii) the few local cases that persist over the summer months, or (iii) the opposite hemisphere, with variants “bouncing” from the temperate north to the temperate south and vice versa. Here, we conduct Bayesian phylogeographic inference (Minin & Suchard 2007; Lemey et al. 2009; Suchard et al. 2018) on geographically representative sets of 1,631 RSV-A and 1,318 RSV-B G glycoprotein sequences. We find that the global migration rates of RSV-A and RSV-B are highly correlated. Moreover, we demonstrate the key role of Southeast Asia, and to a lesser extent, China, in the seeding of annual RSV epidemics. We show that local variation consists of both sequences from the tropics and sequences imported from other temperate regions experiencing contemporaneous epidemics. By elucidating the spatial dissemination of RSV, our work has the potential to inform efforts to forecast local variation.
