Recombinant Chikungunya Virus Wild gp E1 [His] (DAGA-413)

Chikungunya Virus Wild gp E1 [His], Recombinant protein from Drosophila

Product Overview
Chikungunya W.T. gp E1 Recomb.
Chikungunya virus wild type gpE1 Recombinant
a.a. 1-415 of glycoprotein E1 from the wild-type Chikungunya Virus. Contains Histidine tag.
Alternative Names
CHIKV; Chikungunya; insect-borne virus; Alphavirus; Togaviridae; CHIKV E1
> 95% pure (determined by SDS-PAGE). Purified by using immobilized metal-chelate affinity chromatography.
Purified, Liquid
Batch dependent - please inquire should you have specific requirements.
100 µg
Phosphate Buffered Saline, pH 7.4
0.1% Thimerosal
Aliquot and store at < -20°C. Avoid multiple freeze/thaw cycles.
Antigen Description
The virion envelope consists of a lipid bilayer derived from the plasma membrane from the host cell, multiple copies of two major virus encoded glycoproteins E1 and E2, and a small 6K peptide.
CHIKV; Chikungunya; insect-borne virus; Alphavirus; Togaviridae; CHIKV E1; Chikungunya E1; CHIKV envelope; Chikungunya envelope; Wild Type E1 Protein; Mutant (A226V) E1 Protein


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Authors: Wichit, Sineewanlaya; Hamel, Rodolphe; Yainoy, Sakda; Gumpangseth, Nuttamonpat; Panich, Suchawadee; Phuadraksa, Thanawat; Saetear, Phoonthawee; Monteil, Arnaud; Vargas, Ronald Morales; Misse, Dorothee

Chikungunya virus (CHIKV), a re-emerging infectious arbovirus, causes Chikungunya fever that is characterized by fever, skin rash, joint pain, arthralgia and occasionally death. Despite it has been described for 66 years already, neither potential vaccine nor a specific drug is available yet. During CHIKV infection, interferon type I signaling pathway is stimulated and releases hundreds of interferon stimulated genes (ISGs). Our previous study reported that IFI16, a member of ISGs, is up-regulated during CHIKV virus infection and the suppression of the gene resulted in increased virus replication. Furthermore, our group also found that inflammasome activation can inhibit CHIKV infection in human foreskin cells (HFF1). Concomitantly, it has been reported that IFI16 activates the inflammasome to suppress virus infection. Therefore, we have hypothesized that IFI16 could be involved in CHIKV infection. In this study, we confirmed the expression level of IFI16 by Western blotting analysis and found that IFI16 was up-regulated following CHIKV infection in both HFF1 and human embryonic kidney cells. We next investigated its antiviral activity and found that forced expression of IFI16 completely restricted CHIKV infection while endogenous silencing of the gene markedly increased virus replication. Furthermore, we have discovered that IFI16 inhibited CHIKV replication, at least, in cell-to-cell transmission as well as the diffusion step. Interestingly, IFI16 also exerted its antiviral activity against Zika virus (ZIKV) infection, the global threat reemerging virus can cause microcephaly in humans. Taken together, this study provides the first evidence of an antivirus activity of IFI16 during in vitro arbovirus infection, thus expanding its antiviral spectrum that paves the way to further development of antiviral drugs and vaccines.

Peripheral polyneuropathy associated with Chikungunya virus infection


Authors: Silva, Vanessa P.; Costa, Dacylla S.; Carvalho, Vania C. C. V. L.; Garces, Tereza C. C. S.; Barros, Emanuela L. T.; Oliveira, Jefferson S.; Pereira, Anna C. T. C.; Ferreira, Gustavo P.

The Chikungunya virus (CHIKV) is an arbovirus transmitted to humans through mosquito bites and can cause a series of symptoms ranging from a benign febrile illness to severe neurological conditions. We report the identification of CHIKV in a serum sample from an elderly woman with febrile illness and severe arthralgia in Brazil. The occurrence was found of peripheral polyneuropathy affecting the upper and lower limbs evidenced by electroneuromyographic findings. The patient was treated with a corticoid associated with methotrexate, suggesting that the pathophysiological basis of the case in question may be related to an immune-mediated response by T cells and inflammatory cytokines. This finding reinforces the need to be aware of the emergence of neuroinfections related to CHIKV and effective diagnoses for the early detection of neurological alterations, favoring the clinical management of these patients.

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