H5 Influenza DOT-ELISA Kit (DEIA438)

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

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Size
6T, 30T
Sample
avian excretes, nasopharyngeal aspirates, swabs, nasal wash, embryo whole virus inoculation, viral lysates
Species Reactivity
Human, Chick
Intended Use
This kit is an in vitro immunoassay membrane test (Dot-ELISA) for the direct rapid and qualitative detection of hemagglutinin (HA) of Influenza A Virus, H5 strain(also known as highly pathogenic avian influenza) in avian excretes, human nasopharyngeal aspirates, swabs, nasal wash, chicken embryo whole virus inoculation or viral lysates, etc.
Contents of Kit
1. H5-HA (Ag) Immuno-filtration Devices
2. Sample Lysis Bottle
3. Plastic Pipette
4. Virus Lysis Buffer
5. HRP-conjugate
6. Wash Buffer
7. Chromogen Solution
8. Stop Solution
Storage
Store the kit reagents at 2-8°C. Avoid repeated thawing and freezing. For more detailed information, please download the following document on our website.

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References


Zinc Finger CCCH-Type Antiviral Protein 1 Restricts the Viral Replication by Positively Regulating Type I Interferon Response

FRONTIERS IN MICROBIOLOGY

Authors: Zhang, Baoge; Goraya, Mohsan Ullah; Chen, Na; Xu, Lifeng; Hong, Yan; Zhu, Meiyi; Chen, Ji-Long

Zinc finger CCCH-type antiviral protein 1 (ZC3HAV1) is a host antiviral factor that can repress translation and promote degradation of specific viral mRNAs. In this study, we found that expression of ZC3HAV1 was significantly induced by infection with influenza A virus (IAV) and Sendai virus (Sev). It was shown that deficiency of IFNAR resulted in a dramatic decrease in the virus-induced expression of ZC3HAV1. Furthermore, transfection with poly(I:C) and treatment with interferon beta (IFN-beta) induced the ZC3HAV1 expression. Interference with the endogenous expression of ZC3HAV1 enhanced the replication of influenza virus by impairing the production of IFN-beta and MxA, following the infection of influenza virus. In contrast, ectopic expression of ZC3HAV1 significantly restricted the replication of influenza virus by increasing the IFN-beta expression. In addition, ZC3HAV1 also promoted the induction of tumor necrosis factor and interleukin 6. These results suggest that ZC3HAV1 is induced by IFN-beta/IFNAR signaling during IAV and Sev infection and involved in positive regulation of IFN-dependent innate antiviral response.

H2 influenza A virus is not pathogenic in Tmprss2 knock-out mice

VIROLOGY JOURNAL

Authors: Lambertz, Ruth Lydia Olga; Gerhauser, Ingo; Nehlmeier, Inga; Gaertner, Sabine; Winkler, Michael; Leist, Sarah Rebecca; Kollmus, Heike; Poehlmann, Stefan; Schughart, Klaus

The host cell protease TMPRSS2 cleaves the influenza A virus (IAV) hemagglutinin (HA). Several reports have described resistance of Tmprss2(-/-) knock-out (KO) mice to IAV infection but IAV of the H2 subtype have not been examined yet. Here, we demonstrate that TMPRSS2 is able to cleave H2-HA in cell culture and that Tmprss2(-/-) mice are resistant to infection with a re-assorted PR8_HA(H2) virus. Infection of KO mice did not cause major body weight loss or death. Furthermore, no significant increase in lung weights and no virus replication were observed in Tmprss2(-/-) mice. Finally, only minor tissue damage and infiltration of immune cells were detected and no virus-positive cells were found in histological sections of Tmprss2(-/-) mice. In summary, our studies indicate that TMPRSS2 is required for H2 IAV spread and pathogenesis in mice. These findings extend previous results pointing towards a central role of TMPRSS2 in IAV infection and validate host proteases as a potential target for antiviral therapy.

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