Abstract

There is a growing interest in echovirus 30 (E30), an enterovirus responsible for neurological disease and hospitalization. There are multiple studies of outbreaks, but few that study the epidemiology over long periods of time. Our study aims to describe the clinical, epidemiological and microbiological characteristics of a series of E30 infections detected over 26 years. Data were retrospectively collected from a database of all enterovirus infections identified in our laboratory. They were detected by viral isolation or nucleic acid detection in patients presenting with respiratory or neurological infections, rash, sepsis-like syndrome, or gastroenteritis. Enterovirus genotyping was performed by amplification of the VP1 gene using RT-nested PCR, followed by sequencing and BLAST analysis. Of the 2402 enterovirus infections detected, 1619 were linked to at least one genotype and 173 were caused by E30. Clinical information was available for 158 (91.3%) patients. E30 was associated with neurological infection in 107 (67.8%) cases and it was detected almost every year. Phylogenetic analysis was performed with 67 sequences. We observed that E30 strains circulating in Catalonia from 1996 to 2016 belong to two lineages (E and F), although the majority cluster was in F. In 2018, lineage I emerged as the dominant lineage.

Highlights

  • Enteroviruses (EVs) belong to the Picornaviridae family, which currently consists of 68 genera and 158 species

  • This study presents the epidemiology and molecular evolution of the echovirus 30 (E30) detected in a university hospital in Barcelona (Catalonia, Spain) over a period of 26 years

  • This result was to be expected, as E30 is one of the genotypes most frequently associated with aseptic meningitis [34,35], with multiple outbreaks widely documented throughout the world

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Summary

Introduction

Enteroviruses (EVs) belong to the Picornaviridae family, which currently consists of 68 genera and 158 species. The genus Enterovirus consists of 15 species, of which 4 EV species (A, B, C, D), with more than 100 different genotypes, and 3 rhinovirus species (A, B, C) can infect humans. They are small (24–30 nm) non-enveloped viruses, consisting of a single strand of positive polarity RNA acting directly as messenger RNA, and an icosahedral capsid consisting of four proteins (VP1, VP2, VP3, VP4) [1]. Genetic differences in the VP1 polyprotein give rise to the different genotypes [2,3]. Mutations and recombination events are frequent in EVs. Exchanges can occur within the same genotype or between different genotypes, contributing to the creation of variants and the evolution of EVs [4,5]

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