Molecular and serological characterization of sporadic acute hepatitis E in a Japanese patient infected with a genotype III hepatitis E virus in 1993

Tokita, Hajime; Harada, Hideharu; Gotanda, Yuhko; Takahashi, Masaharu; Nishizawa, Tsutomu; Okamoto, Hiroaki

doi:10.1099/vir.0.18802-0

Cited by 43 publications

(34 citation statements)

References 40 publications

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“…As a consequence, the prevalence of HEV infection could be understimated. IgA type anti-HEV antibody can be utilized as an additional confirmatory antibody for recent HEV infection Tokita et al 2003), and this case demonstrated positive reaction for it in an examination of stocked sera at admission. Also, although judged as negative, the titer of IgM type anti-HEV was weakly reactive on admission and was decreased after time course (Table 3).…”

Section: Discussionmentioning

confidence: 99%

A Patient with Clinical Features of Acute Hepatitis E Viral Infection and Autoimmune Hepatitis

Nagasaki

Ueno

Mano

et al. 2005

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 99%

A Patient with Clinical Features of Acute Hepatitis E Viral Infection and Autoimmune Hepatitis

Nagasaki

Ueno

Mano

et al. 2005

Tohoku J. Exp. Med.

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“…HEV is a small virus that causes an acute self-limiting infection, even in the face of a robust antiviral immune response (7,42). Previous studies carried out by us and others have shown that the HEV ORF3 protein regulates cellular processes and has three broad roles.…”

Section: Discussionmentioning

confidence: 99%

The ORF3 Protein of Hepatitis E Virus Delays Degradation of Activated Growth Factor Receptors by Interacting with CIN85 and Blocking Formation of the Cbl-CIN85 Complex

Chandra

Kalia

Hajela

et al. 2010

J Virol

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Hepatitis E virus (HEV) causes an acute self-limiting disease that is endemic in developing countries.Previous studies suggested that the ORF3 protein (pORF3) of HEV is required for infection in vivo and is likely to modulate the host response. Our previous work showed that pORF3 localizes to early and recycling endosomes and causes a delay in the postinternalization trafficking of epidermal growth factor receptor (EGFR) to late endosomes/lysosomes. Here we report that pORF3 also delays the trafficking and degradation of activated hepatocyte growth factor receptor (c-Met) and delineate the mechanistic details of these effects. A mutant ORF3 protein, which does not localize to endosomes, also showed similar effects on growth factor receptor trafficking, making this effect independent of the endosomal localization of pORF3. The ORF3 protein was found to interact with CIN85, a multidomain adaptor protein implicated in the Cbl-mediated downregulation of receptor tyrosine kinases. This interaction competed with the formation of the growth factor receptorCbl-CIN85 complex, resulting in the reduced ubiquitination of CIN85 and trafficking of the growth factor receptor complex toward late endosomes/lysosomes. We propose that through its effects on growth factor receptor trafficking, pORF3 prolongs endomembrane growth factor signaling and promotes cell survival to contribute positively to viral replication and pathogenesis.Hepatitis E virus (HEV) is a waterborne pathogen and the causative agent of hepatitis E. It is transmitted feco-orally and causes large outbreaks as well as sporadic disease (21, 37). While this disease is endemic in developing countries of Asia, Africa, and South America, significant levels of seropositivity in residents of developed countries have also been observed, which is possibly linked to the zoonotic transmission of HEV (25,34). It is estimated that about 2 billion people, one-third of the world's population, live in areas where HEV infection is endemic (1). Although the disease is generally self-limited, fulminant hepatitis with increased mortality has been reported for a small fraction of patients, especially pregnant women (17,33). Recently classified as the only member of the genus Hepevirus of the family Hepeviridae, HEV has a 7.2-kb capped, polyadenylated, positive-sense RNA genome that contains three open reading frames (ORFs). The orf1 gene encodes a viral nonstructural polyprotein, orf2 codes for the viral capsid protein, and orf3 encodes a small protein that is proposed to optimize the host cell environment for viral replication (5,6,16,18,30,31). A role for pORF3 in the release of HEV from infected cells was also proposed recently (46). While orf3 appears to be dispensable for HEV replication in replicon-transfected cells (9), it was required for the in vivo infection of monkeys experimentally infected by the intrahepatic inoculation of the viral RNA genome (10). The requirement of pORF3 for infectivity in pigs inoculated with HEV was also demonstrated previously (15).The orf3 gene o...

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“…HEV-specific IgA has been detected in sera from acute-HEV patients, and the presence of HEV-specific IgA in combination with IgM was found to be highly specific for the serodiagnosis of acute HEV infections (4,11,16,19,21,22). As the duration of the IgA response seemed limited (19), it was suggested that anti-HEV IgA detection may be useful to discriminate acute and past infections for serological diagnosis of recent (subclinical) HEV infection (15).…”

Section: Hepatitis E Virus (Hev) Infections Are Recognized In Thementioning

confidence: 99%

Detection of Hepatitis E Virus-Specific Immunoglobulin A in Patients Infected with Hepatitis E Virus Genotype 1 or 3

Herremans

Duizer

Jusic

2007

Clin Vaccine Immunol

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Currently, diagnosis of acute hepatitis E virus (HEV) in patients is primarily based on anti-HEV immunoglobulin M (IgM) detection. However, several investigations suggest the use of HEV-specific IgA for diagnosing acute HEV infections. We evaluated two commercially available assays, an IgA enzymelinked immunosorbent assay (ELISA) (Diacheck) and an adapted immunoblot protocol (Mikrogen) for IgA detection and compared the performance in genotype 1-and 3-infected patients. The specificity of the IgA assays was high, with no positive reactions in a control group of 18 acute hepatitis patients who were negative for HEV. The sensitivity calculated in nine PCR-positive type 1-infected patients was 100% in both assays but was clearly lower in genotype 3-infected patients (n ‫؍‬ 14), with sensitivities of only 67% and 57% for the ELISA and immunoblot assay, respectively. The lower IgA responses detected in genotype 3-infected patients could be caused by the use of only the genotype 1 and 2 antigens in the serological assays. Interestingly in two patients with possible infection through blood transfusion no response or intermediate IgA responses were detected, and this might confirm the parenteral route of transmission. In both the type 1-and type 3-infected patients both the IgA and IgM responses disappeared simultaneously. We conclude that IgA detection is of limited value for the serodiagnosis of acute HEV cases, particularly with genotype 3.

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Molecular and serological characterization of sporadic acute hepatitis E in a Japanese patient infected with a genotype III hepatitis E virus in 1993

Cited by 43 publications

References 40 publications

A Patient with Clinical Features of Acute Hepatitis E Viral Infection and Autoimmune Hepatitis

A Patient with Clinical Features of Acute Hepatitis E Viral Infection and Autoimmune Hepatitis

The ORF3 Protein of Hepatitis E Virus Delays Degradation of Activated Growth Factor Receptors by Interacting with CIN85 and Blocking Formation of the Cbl-CIN85 Complex

Detection of Hepatitis E Virus-Specific Immunoglobulin A in Patients Infected with Hepatitis E Virus Genotype 1 or 3

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