Abstract

In 2018, an upsurge in echovirus 30 (E30) infections was reported in Europe. We conducted a large-scale epidemiologic and evolutionary study of 1,329 E30 strains collected in 22 countries in Europe during 2016–2018. Most E30 cases affected persons 0–4 years of age (29%) and 25–34 years of age (27%). Sequences were divided into 6 genetic clades (G1–G6). Most (53%) sequences belonged to G1, followed by G6 (23%), G2 (17%), G4 (4%), G3 (0.3%), and G5 (0.2%). Each clade encompassed unique individual recombinant forms; G1 and G4 displayed >2 unique recombinant forms. Rapid turnover of new clades and recombinant forms occurred over time. Clades G1 and G6 dominated in 2018, suggesting the E30 upsurge was caused by emergence of 2 distinct clades circulating in Europe. Investigation into the mechanisms behind the rapid turnover of E30 is crucial for clarifying the epidemiology and evolution of these enterovirus infections.

Highlights

  • Our molecular characterization enabled an analysis of the recombination events occurring during echovirus 30 (E30) diversification in Europe, which can be conducted only when dealing with a single infection

  • Our study used a large EV sequence dataset collected worldwide, comprising 1,329 E30 sequences collected from 22 countries in Europe during 2016–2018 and was made possible due to the large-scale collaboration between countries through European Non-Polio Enterovirus Network (ENPEN) and European Centre for Disease Prevention and Control (ECDC)

  • The upsurge in 2018 was caused by appearance of several different clades or genogroups of E30 viruses; G1 in GGII [7] and G6 in a novel genogroup, GGIII, which we propose in this study

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Summary

Introduction

Recombination results in the generation of novel recombinant forms (RFs) that are chimaeras of E30-derived structural genes with NSP, 5′ UTR sequences, or both, which are derived from cocirculating E30 strains or other EV-B types, such as E9 and E11 [10,11,12,14,17,18]. The role of VP1 sequence change, recombination, and other factors driving phenotypic changes in virus transmissibility or pathogenicity, and the contributions of changes in population immunity, are crucial for clarifying the underlying causes of E30 outbreaks and upsurges in cases [15,19,20,21,22]

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