Genetic changes in hepatitis E virus of subtype 1a in patients with sporadic acute hepatitis E in Kathmandu, Nepal, from 1997 to 2002

Shrestha, Santosh Man; Tsuda, Fumio; Nishizawa, Tsutomu; Takahashi, Masaharu; Gotanda, Yuhko; Okamoto, Hiroaki

doi:10.1099/vir.0.19571-0

Cited by 29 publications

(21 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, genotype 1a/1c coinfections were documented in 2 people hospitalized in Kathmandu, Nepal (255,256). While HEV-4 has been amplified from serum, liver, and stool samples from swine in India (107,114,161,162,257), there have been no reports of human coinfection with both HEV-1 and -4.…”

Section: Coinfection With Multiple Hev Strainsmentioning

confidence: 99%

Host Immune Status and Response to Hepatitis E Virus Infection

2014

View full text Add to dashboard Cite

SUMMARY Hepatitis E virus (HEV), identified over 30 years ago, remains a serious threat to life, health, and productivity in developing countries where access to clean water is limited. Recognition that HEV also circulates as a zoonotic and food-borne pathogen in developed countries is more recent. Even without treatment, most cases of HEV-related acute viral hepatitis (with or without jaundice) resolve within 1 to 2 months. However, HEV sometimes leads to acute liver failure, chronic infection, or extrahepatic symptoms. The mechanisms of pathogenesis appear to be substantially immune mediated. This review covers the epidemiology of HEV infection worldwide, the humoral and cellular immune responses to HEV, and the persistence and protection of antibodies produced in response to both natural infection and vaccines. We focus on the contributions of altered immune states (associated with pregnancy, human immunodeficiency virus [HIV], and immunosuppressive agents used in cancer and transplant medicine) to the elevated risks of chronic infection (in immunosuppressed/immunocompromised patients) and acute liver failure and mortality (among pregnant women). We conclude by discussing outstanding questions about the immune response to HEV and interactions with hormones and comorbid conditions. These questions take on heightened importance now that a vaccine is available.

show abstract

Section: Coinfection With Multiple Hev Strainsmentioning

confidence: 99%

Host Immune Status and Response to Hepatitis E Virus Infection

2014

View full text Add to dashboard Cite

show abstract

“…HEV has been classified further into four major genotypes (I to IV) (39). Genotype I includes Asian strains from India, Burma, Nepal, China, and Pakistan (3,4,13,31,40,44,49,55) and African strains from Chad, Algeria, Tunisia, Morocco, Egypt, and Namibia (6,18,26,48,54). Genotype II includes U.S., Japanese, and European strains (38,43,60).…”

mentioning

confidence: 99%

Evidence of Recombination between Divergent Hepatitis E Viruses

Cuyck¹,

Fan

Robertson

et al. 2005

J Virol

View full text Add to dashboard Cite

Phylogenetic and recombination analysis was performed on 32 complete hepatitis E virus (HEV) genomes from infected humans and pigs. For the first time, evidence for recombination between divergent HEV strains was obtained, with at least two strains being found to have discordant phylogenetic relationships consistent with the occurrence of intragenotype recombination. This finding confirms that humans can be dually infected with divergent HEV strains and has implications for the emergence and evolution of new HEV epidemics.Hepatitis E virus (HEV) is a causative agent of enterically transmitted hepatitis disease and, apart from infections of pregnant women, is generally associated with low mortality (11,17). Outbreaks of HEV have been described to occur in many regions of the world, including Asia, Africa, and Mexico (1, 33, 53), while sporadic cases have been documented in the United States, Africa (9), and Europe (27,37,38,60). HEV is presumed to be a zoonotic disease, as surveys of both wild and domestic animals have found evidence for human-related HEVs in rats (12, 22), pigs (2,7,21,29,32,56), deer (45), and wild boar (41). Direct animal-to-human transmission of HEV has been demonstrated, for example, from deer to human as a result of eating uncooked meat (45). Interestingly, HEV characterized from swine in countries where HEV is not endemic is usually closely related to cases of sporadic human HEVs from the same country, for example, in the United States and Japan (29,30,42,57), while in India, where HEV is endemic, human and swine HEV strains are not closely related (2). This suggests that in certain regions HEV is more established in the human population and that in other regions HEV is emerging as a result of direct contact with animal reservoirs for the virus. Divergent HEVs with no human counterparts have also been found in chickens (avian HEV). Avian HEV shares only 50 to 60% nucleotide sequence identity with HEV from humans and swine (15,16).HEV is a positive single-stranded RNA virus that is approximately 7,200 nucleotides (nt) in length. HEV's genome is capped and polyadenylated and has three open reading frames (ORF) (Fig. 1). As the organization of HEV's genome resembles that of Caliciviridae, at one time it was considered a mem-FIG. 1. Genomic organization of HEV. The scale at the bottom of the figure corresponds to nucleotides (in thousands). ORF1 encodes a nonstructural polyprotein which provides guanylyl-methyltransferase and RNA-dependent RNA polymerase activities and possibly other functions (23,25). The ORF2 and ORF3 proteins are believed to be encoded by individual subgenomic RNAs generated during replication (44, 58). ORF2 encodes the viral capsid protein; ORF3, which contains one potential phosphorylation site, encodes a very small protein of about 123 amino acids (59). ORF3 proteins partition with the cytoskeleton, and it has been suggested that an interaction between ORF2 and ORF3 is associated with the assembly of virions (47,50). ORF3 is also believed to interact with proteins involv...

show abstract

“…Patients with AH seen in the period 2002 to 2008 had laboratory tests that included serum bilirubin, ALT and AP, total and differential WBC count and serological or molecular markers of known viral hepatitis. 10,11 The hepatitis viral markers tested were anti- As the condition is seen only in developing countries and as its clinical features simulate that of subacute type of hepatic vena cava syndrome (HVCS) 13 we looked for evidence of bacterial infection and ultrasonographic (US) Patients that showed 'recent' thrombus on thickened posterior wall of the IVC near cavoatrial junction or a long segment were diagnosed acute hepatic vena cava disease (HVCS). 13 Chronic HVCS was diagnosed in the presence of localized stenosis/obstruction of the IVC; 15 and acute on chronic lesion when 'recent' thrombus occurred in patient with chronic lesion with old organized thrombus (Figs 1A and B).…”

Section: Methodsmentioning

confidence: 99%

“…23 The study of genetic changes based on observation of 412-nt sequences within ORF2 of HEV among 116 HEV-viremic samples from Nepal obtained at different periods from 1997 to 2002 showed no significant amino acid substitution. 11 Further, only three out of 15 HE patients with SAHF were viremic and they all belonged to genotype 1. One fatal case of SAHF due to HA was not viremic.…”

Section: Thus the Question Arises What Is This Entity Called Sahf? Anmentioning

confidence: 99%