Recombination analysis reveals a double recombination event in hepatitis E virus

Wang, Hua; Zhang, Wen; Ni, Bin; Shen, Han‐Xi; Song, Yuyu; Wang, Xiaochun; Shao, Shihe; Hua, Xiuguo; Cui, Li

doi:10.1186/1743-422x-7-129

Cited by 40 publications

(35 citation statements)

References 29 publications

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“…Following exploratory analyses to determine whether recombination detection was simply an artifact of complex patterns of mutations, a sequence was deemed recombinant if three or more methods had reported it as a recombinant. In agreement with prior reports of recombination in HEV (26,76,77), we identified 14 recombinant viruses, including novel recombinants (Table 6).…”

Section: Genotype-specific Evolution Of Hepatitis E Virussupporting

confidence: 79%

Genotype-Specific Evolution of Hepatitis E Virus

Brayne

Dearlove

Lester

et al. 2017

J Virol

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Hepatitis E virus (HEV) is the most common cause of acute viral hepatitis globally. HEV comprises four genotypes with different geographic distributions and host ranges. We utilize this natural case-control study for investigating the evolution of zoonotic viruses compared to single-host viruses, using 244 near-full-length HEV genomes. Genome-wide estimates of the ratio of nonsynonymous to synonymous evolutionary changes (dN/dS ratio) located a region of overlapping reading frames, which is subject to positive selection in genotypes 3 and 4. The open reading frames (ORFs) involved have functions related to host-pathogen interaction, so genotype-specific evolution of these regions may reflect their fitness. Bayesian inference of evolutionary rates shows that genotypes 3 and 4 have significantly higher rates than genotype 1 across all ORFs. Reconstruction of the phylogenies of zoonotic genotypes demonstrates significant intermingling of isolates between hosts. We speculate that the genotype-specific differences may result from cyclical adaptation to different hosts in genotypes 3 and 4.IMPORTANCE Hepatitis E virus (HEV) is increasingly recognized as a pathogen that affects both the developing and the developed world. While most often clinically mild, HEV can be severe or fatal in certain demographics, such as expectant mothers. Like many other viral pathogens, HEV has been classified into several distinct genotypes. We show that most of the HEV genome is evolutionarily constrained. One locus of positive selection is unusual in that it encodes two distinct protein products. We are the first to detect positive selection in this overlap region. Genotype 1, which infects humans only, appears to be evolving differently from genotypes 3 and 4, which infect multiple species, possibly because genotypes 3 and 4 are unable to achieve the same fitness due to repeated host jumps. KEYWORDS evolution, evolutionary biology, genotypic identification, hepatitis E virus, positive selection H epatitis E virus (HEV) is a nonenveloped single-stranded positive-sense RNA virus that infects approximately 20 million people globally each year (1). It causes large propagated epidemics of acute hepatitis in Asia and Africa, as well as low-level, sporadic, food-associated infections in the developed world (2, 3). Its pathogenicity ranges from acute liver failure and mortality rates as high as 20% in some subpopulations (for example, in pregnant women) to apparently asymptomatic infections in others (4). Acquired via the fecal-oral route, HEV is associated with poor hygiene and living conditions. It can also be acquired by eating contaminated food, including infected artiodactyls (swine, deer, and boar) and shellfish (4-6).Mammalian HEV exists in four internationally recognized genotypes (7). Genotyping is based on nucleotide divergence in the capsid open reading frame (ORF) (8) and on whole-genome phylogenetic analysis (9). Genotypes differ at the epidemiological (distribution, hosts) and virological (pathogenicity, translation mecha...

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Section: Genotype-specific Evolution Of Hepatitis E Virussupporting

confidence: 79%

Genotype-Specific Evolution of Hepatitis E Virus

Brayne

Dearlove

Lester

et al. 2017

J Virol

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“…Sequences were removed from the data set if there was evidence that they were recombinant (GenBank accession numbers DQ450072, D11093, and AF051830) (19)(20)(21), if they differed from any other sequence in the data set by Ͻ2% of nucleotide positions (excluding the hypervariable region [HVR]). This left a total of 108 sequences (accession numbers FJ906896, JQ013793, JQ013791, JQ013792, FJ906895, GU937805, AB291960, AB291953, JN564006, JQ013795, JQ013794, AF060669, AY575857, AB074920, AB481228, AB630970, AB091394, AB369691, AB591734, AB089824, AB073912, AB290312, FJ705359, AB222184, AP003430, FJ998008, AB481229, AB630971, AB291962, AB291963, AB246676, AB591733, AB189070, AB222182, AY115488, AB236320, AB222183, FJ527832, AF455784, FJ426403, FJ426404, AF060668, AB369689, AB290313, FJ653660, FJ956757, AB248522, EU360977, EU723512, AB481226, AB291961, EU375463, EU495148, EU723514, AB248520, EU723516, AB369687, EU723513, HM055578, FJ998015, AY594199, AB253420, AJ272108, HM152568, GU206559, AB074915, FJ610232, GU361892, EU366959, HQ634346, EF077630, AB197674, GU119960, AB197673, FJ763142, GU119961, GU188851, AY723745, EU676172, HM439284, DQ279091, AB108537, AB220974, AB369688, AB602441, AB573435, EF570133, JF915746, AB369690, AB602440, AB481227, AB193176, AB080575, AB161719, AB291967, M80581, M94177, X98292, M73218, AF459438, FJ457024, AF076239, X99441, AF185822, DQ459342, AY204877, AY230202, and M74506), to which were added sequences of HEV-like variants from chickens (accession numbers JN997392, AM943646, GU954430, AY535004, EF206691, JN597006, and AM943647), rats (accession numbers GU345042, GU345043, JN167537, and JN167538), bats (accession numbers JQ001749 and NC_018382), ferrets (accession numbers JN998606 and JN998607), and cutthroat trout (accession number HQ731075).…”

Section: Methodsmentioning

confidence: 99%

Genetic Variability and the Classification of Hepatitis E Virus

Smith

Purdy

Simmonds

2013

J Virol

127

111

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bThe classification of hepatitis E virus (HEV) variants is currently in transition without agreed definitions for genotypes and subtypes or for deeper taxonomic groupings into species and genera that could incorporate more recently characterized viruses assigned to the Hepeviridae family that infect birds, bats, rodents, and fish. These conflicts arise because of differences in the viruses and genomic regions compared and in the methodology used. We have reexamined published sequences and found that synonymous substitutions were saturated in comparisons between and within virus genotypes. Analysis of complete genome sequences or concatenated ORF1/ORF2 amino acid sequences indicated that HEV variants most closely related to those infecting humans can be consistently divided into six genotypes (types 1 to 4 and two additional genotypes from wild boar). Variants isolated from rabbits, closely related to genotype 3, occupy an intermediate position. No consistent criteria could be defined for the assignment of virus subtypes. Analysis of amino acid sequences from these viruses with the more divergent variants from chickens, bats, and rodents in three conserved subgenomic regions (residues 1 to 452 or 974 to 1534 of ORF1 or residues 105 to 458 of ORF2) provided consistent support for a division into 4 groups, corresponding to HEV variants infecting humans and pigs, those infecting rats and ferrets, those from bats, and those from chickens. This approach may form the basis for a future genetic classification of HEV into four species, with the more divergent HEV-like virus from fish (cutthroat trout virus) representing a second genus.

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“…Inter-and intragenomic recombination for HEV has been reported only rarely (23). Therefore it is quite remarkable that a human RNA sequence was acquired in the passage 6 virus.…”

Section: Discussionmentioning

confidence: 99%

Cross-species infections of cultured cells by hepatitis E virus and discovery of an infectious virus–host recombinant

Shukla

Nguyen

Torian

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

275

335

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The RNA virus, hepatitis E virus (HEV) is the most or second-most important cause of acute clinical hepatitis in adults throughout much of Asia, the Middle East, and Africa. In these regions it is an important cause of acute liver failure, especially in pregnant women who have a mortality rate of 20–30%. Until recently, hepatitis E was rarely identified in industrialized countries, but Hepatitis E now is reported increasingly throughout Western Europe, some Eastern European countries, and Japan. Most of these cases are caused by genotype 3, which is endemic in swine, and these cases are thought to be zoonotically acquired. However, transmission routes are not well understood. HEV that infect humans are divided into nonzoonotic (types 1, 2) and zoonotic (types 3, 4) genotypes. HEV cell culture is inefficient and limited, and thus far HEV has been cultured only in human cell lines. The HEV strain Kernow-C1 (genotype 3) isolated from a chronically infected patient was used to identify human, pig, and deer cell lines permissive for infection. Cross-species infections by genotypes 1 and 3 were studied with this set of cultures. Adaptation of the Kernow-C1 strain to growth in human hepatoma cells selected for a rare virus recombinant that contained an insertion of 174 ribonucleotides (58 amino acids) of a human ribosomal protein gene.

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Recombination analysis reveals a double recombination event in hepatitis E virus

Cited by 40 publications

References 29 publications

Genotype-Specific Evolution of Hepatitis E Virus

Genotype-Specific Evolution of Hepatitis E Virus

Genetic Variability and the Classification of Hepatitis E Virus

Cross-species infections of cultured cells by hepatitis E virus and discovery of an infectious virus–host recombinant

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