Anti-CHIKV Env monoclonal antibody (CABT-B8658)

Specifications


Host Species
Mouse
Antibody Isotype
IgG1, κ
Clone
IN449
Species Reactivity
CHIKV
Immunogen
Recombinant Chikungunya Virus Envelope Protein
Conjugate
Unconjugated

Target


Alternative Names
Chikungunya Virus Envelope Protein

Citations


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We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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References


Viperin controls chikungunya virus-specific pathogenic T cell IFN gamma Th1 stimulation in mice

LIFE SCIENCE ALLIANCE

Authors: Carissimo, Guillaume; Teo, Teck-Hui; Chan, Yi-Hao; Lee, Cheryl Yi-Pin; Lee, Bernett; Torres-Ruesta, Anthony; Tan, Jeslin J. L.; Chua, Tze-Kwang; Fong, Siew-Wai; Lum, Fok-Moon; Ng, Lisa F. P.

Chikungunya virus (CHIKV) has been a worldwide threat since its reemergence in La Reunion Island in 2004. Expression of the interferon-stimulated protein Viperin correlates with viral load burden in patients, and studies in mice have demonstrated its role to limit disease severity against CHIKV infection. Using Viperin(-/-) mice, we aimed to understand the contribution of Viperin to the T-cell immune response against CHIKV. CD4 T-cell depletion in Viperin(-/-) mice showed that increased late acute joint inflammation (5-8 d postinfection) was exclusively mediated by T cells. Specifically, CHIKV-infected Viperin(-/-) mice showed an increased INF gamma Th1 profile of CD4 T cells, enhanced INF gamma stimulation by APCs, an increased INF gamma secretion profile in the joint micro-environment, and increased numbers of inflammatory monocytes in virus-infected joints compared with WT mice. Bone marrow grafting experiments showed that Viperin expression in both hematopoietic and non-hematopoietic cells is instrumental in reducing disease severity associated with a CD4 T-cell response.

Systematic review of factors associated with the development of Guillain-Barre syndrome 2007-2017: what has changed?

TROPICAL MEDICINE & INTERNATIONAL HEALTH

Authors: Wachira, Virginia Kagure; Peixoto, Henry Maia; Fernandes de Oliveira, Maria Regina

Objective The objective of this study was to describe the factors associated with the development of Guillain-Barre syndrome, both infectious and non-infectious, during and after the A(H1N1) influenza pandemic in 2009 and the recent Zika virus epidemic in the Americas. Method Systematic review of literature on factors associated with the development of the Guillain-Barre syndrome published between 2007 and 2017 listed in EBSCO, MEDLINE and LILACS databases. The quality of the studies was evaluated using the Newcastle Ottawa Scale. Results Thirty-four articles met inclusion criteria and were selected for analysis. Their quality was considered good in relation to most of the items evaluated. Many aetiological agents had the results of association with Guillain-Barre syndrome, among them Campylobacter jejuni, influenza vaccine - both pandemic and seasonal vaccines, respiratory infection, gastrointestinal infection among others. The aetiological agents found are, in most part, the same reported prior to the study period. The association with surgeries, chikungunya virus (CHIKV), Zika virus and quadrivalent human papillomavirus vaccine stand out as new aetiological agents in the list of the various possible agents that trigger Guillain-Barre syndrome reported in the study period. There were no Brazilian studies identified during this period. Conclusions The results of the review reaffirmed C. jejuni as the major trigger of GBS, whereas the association of influenza vaccines and GBS is less clear; Zika virus infection in association with GBS was found in only one study.

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