Antigen to Hepatitis E Virus, HEV-Ag ELISA Kit (DEIA077)

Regulatory status: For research use only, not for use in diagnostic procedures.

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serum, plasma
Species Reactivity
Intended Use
HEV-Ag ELISA is anenzyme-linked immunosorbent assay for qualitative determination of hepatitis E virus antigen in human serum or plasma samples. The assay is intended to beused in clinical laboratories for diagnosis and management of patients related to infection with hepatitis E virus.
Contents of Kit
1. Microplate
2. Negative Control
3. Positive Control
4. HRP-Conjugate Antigen
5. TMB Solution A
6. TMB Solution B
7. TMB Stop Solution
8. Wash Buffer (20X)
Store the kit reagents at 2-8°C. For more detailed information, please download the following document on our website.


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On the Host Side of the Hepatitis E Virus Life Cycle


Authors: Oechslin, Noemie; Moradpour, Darius; Gouttenoire, Jerome

Hepatitis E virus (HEV) infection is one of the most common causes of acute hepatitis in the world. HEV is an enterically transmitted positive-strand RNA virus found as a non-enveloped particle in bile as well as stool and as a quasi-enveloped particle in blood. Current understanding of the molecular mechanisms and host factors involved in productive HEV infection is incomplete, but recently developed model systems have facilitated rapid progress in this area. Here, we provide an overview of the HEV life cycle with a focus on the host factors required for viral entry, RNA replication, assembly and release. Further developments of HEV model systems and novel technologies should yield a broader picture in the future.

Hepatitis E Virus: How It Escapes Host Innate Immunity


Authors: Lhomme, Sebastien; Migueres, Marion; Abravanel, Florence; Marion, Olivier; Kamar, Nassim; Izopet, Jacques

Hepatitis E virus (HEV) is a leading cause of viral hepatitis in the world. It is usually responsible for acute hepatitis, but can lead to a chronic infection in immunocompromised patients. The host's innate immune response is the first line of defense against a virus infection; there is growing evidence that HEV RNA is recognized by toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), leading to interferon (IFN) production. The IFNs activate interferon-stimulated genes (ISGs) to limit HEV replication and spread. HEV has developed strategies to counteract this antiviral response, by limiting IFN induction and signaling. This review summarizes the advances in our knowledge of intracellular pathogen recognition, interferon and inflammatory response, and the role of virus protein in immune evasion.

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