Abstract
Infection with hepatitis E virus (HEV) can be clinically inapparent or produce symptoms and signs of hepatitis of varying severity and occasional fatality. This variability in clinical outcomes may reflect differences in host susceptibility or the presence of virally encoded determinants of pathogenicity. Analysis of complete genome sequences supports the division of HEV genotype 3 (HEV-3) variants into three major clades: 3ra comprising HEV isolates from rabbits, and 3efg and 3abchij comprising the corresponding named subtypes derived from humans and pigs. Using this framework, we investigated associations between viral genetic variability of HEV-3 in symptomatic and asymptomatic infections by comparing HEV-3 subgenomic sequences previously obtained from blood donors with those from patients presenting with hepatitis in the UK (54 blood donors, 148 hepatitis patients), the Netherlands (38 blood donors, 119 hepatitis patients), France (24 blood donors, 55 hepatitis patients) and Germany (14 blood donors, 36 hepatitis patients). In none of these countries was evidence found for a significant association between virus variants and patient group (P>0.05 Fisher's exact test). Furthermore, within a group of 123 patients in Scotland with clinically apparent HEV infections, we found no evidence for an association between variants of HEV-3 and disease severity or alanine aminotransferase level. The lack of detectable virally encoded determinants of disease outcomes in HEV-3 infection implies a more important role for host factors in its clinical phenotype.
Highlights
Infection with hepatitis E virus (HEV) is clinically silent in most individuals
HEV genotype 3 (HEV-3) displays considerable diversity and various authors have proposed, sometimes contradictory, classification schemes that assign these to different subtypes (Lu et al, 2006; Xia et al, 2008) or groups (Ijaz et al, 2014; Oliveira-Filho et al, 2013)
Phylogenetic analysis of HEV-3 complete genome sequences suggests an initial division of HEV-3 into three clades (Fig. 1) comprising 3ra, variants first isolated from rabbits, and clades 3efg and 3abchij that derive from humans, pigs, wild boar or deer
Summary
Infection with hepatitis E virus (HEV) is clinically silent in most individuals. Serological evidence of HEV infection is present in 13% of the population of England. The GenBank/EMBL/DDBJ accession numbers for the sequences reported here are KP835485–KP835511, KR340493–KR340578 and KT119521–KT119531. The number of acute HEV infections reported annually in this population is currently v1000, implying that 99% of primary infections remain undiagnosed and are not associated with overt or currently recognized signs of disease.
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