Molecular Epidemiology of Human Enterovirus 71 in the United Kingdom from 1998 to 2006

Abstract

The last decade witnessed a significant increase in epidemic activity of human enterovirus 71 (EV71) in the Western Pacific Region (WPR). In most European countries, this risk is unrecognized despite occasional cases of severe disease and two severe outbreaks in Eastern Europe 30 years ago. In this study we report the first examination of the molecular epidemiology of EV71 in the United Kingdom from 1998 to 2006. Genomic regions encoding the 1D coat protein (VP1) and 3D polymerase (Pol) from 32 EV71 isolates associated with neurological or cutaneous manifestations were sequenced. Phylogenetic analyses of VP1 and 3D Pol sequences identified genotype C as the dominant strain. Several United Kingdom isolates had genetic linkages with predated C1 or C2 strains from Europe and the WPR. Recombination events were not detected between United Kingdom strains. However, a previously published Taiwanese strain was identified as an intergenotypic recombinant. EV71 genotype C appears to have continuous circulation in the United Kingdom from 1998 to 2006 with repeated introductions of new strains replacing previous strains. It is necessary to continuously monitor the molecular evolution and recombination events of EV71.

Phylogenetic evidence for a recent spread of two populations of human enterovirus 71 in European countries

“…In contrast to the epidemiological features observed for genogroup C viruses in the West Pacific region, the circulation of these viruses in Europe was not associated with epidemics over the last 30 years. The EV-71 infections in the patients from Austria, France and Germany were sporadic, mainly associated with mild illnesses including HFMD, and were similar to those described earlier in the UK, the Netherlands and Hungary (Bible et al, 2008;van der Sanden et al, 2009;Kapusinszky et al, 2010). However, among the patients included in our study, a syndrome of fatal acute respiratory distress was reported in an infant with an EV-71 C1 infection and in a young child with a C2 virus infection (Vallet et al, 2009 This observation explains the differences between the proportions of the C1 and C2 strains in our study (49.4 % and 42.4 %, respectively) and those (78 % and 12 %) reported in an earlier study (Bible et al, 2008), which included viruses collected during the period 1998-2006.…”

“…A sequence reported earlier (GenBank accession no. AF119795) comprising a known recombination event (Bible et al, 2008) was used as a positive control. The RDP analysis indicated statistical evidence for the presence of recombination breakpoints in only one 1D sequence which was subsequently excluded.…”

“…Longitudinal studies performed in Taiwan suggested that outbreaks occurred after a short virus circulation period of 2-5 years, and that antigenic changes may contribute to the efficient spread of new subgenogroups in the human population (Huang et al, 2009). In European countries, where no epidemic activity has been recorded since the outbreaks in the 1970s, C1, C2 and C4 viruses have been detected (Bible et al, 2008;Diedrich et al, 2009;Ortner et al, 2009;van der Sanden et al, 2009), which raises concerns about the spread of a virus variant that could cause a large outbreak of HFMD resulting in severe neurological cases.…”

Modelling the effects of contaminated environments on HFMD infections in mainland China

“…Hence, in our model the infected individuals are divided into two subgroups (symptomatic and asymptomatic). Moreover, enteroviruses have a strong infectivity, the pathogens being capable of surviving for long periods in suitable conditions outside the host (Chung et al, 2001;Bible et al, 2008;Han et al, 2010). So contaminated environments are also important sources from which it is possible for susceptible to become infected.…”

“…Susceptible infants are usually infected by close contact with infected individuals. Note that the pathogen of EV71 can survive for a long period outside the host in suitable conditions (Chung et al, 2001;Bible et al, 2008;Han et al, 2010) and even 75% alcohol can not eliminate the virus. HFMD patients and asymptomatic recessive individuals, releasing virus to the environment, are the major infectious sources but there is also some evidence that susceptible individuals can be infected via touching free-living pathogens in the environment.…”