Human Influenza B HA ELISA Kit

Name: Human Influenza B HA ELISA Kit
SKU: DEIA249
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

Plasma, tissue homogenates and other biological fluids.

Species Reactivity

Human

Detection Method

sELISA

Intended Use

The influenza B HA ELISA Pair Set is for the quantitative determination of influenza B HA.
This ELISA Pair Set contains the basic components required for the development of sandwich ELISAs.

Contents of Kit

Capture Antibody: 0.5 mg/mL of mouse anti-influenza B HA monoclonal antibody (in PBS, pH 7.4). Dilute to a working concentration of 2 μg/mL in PBS before coating.
Detection Antibody: 0.2 mg/mL rabbit anti-influenza B HA polyclonal antibody conjugated to horseradish-peroxidase (HRP) (in PBS, 50 % HRP-Protector, pH 7.4). Dilute to working concentration of 0.5 μg/mL in detection antibody dilution buffer before use.
Standard: Each vial contains 145 ng of recombinant influenza B HA. Reconstitute with 1 mL detection antibody dilution buffer. After reconstitution, store at -20°C to -80°C in a manual defrost freezer. A seven-point standard curve using 2-fold serial dilutions in sample dilution buffer, and a high standard of 4 ng/mL is recommended.

Storage

Capture Antibody: Aliquot and store at -20°C to -80°C for up to 6 months from date of receipt. Avoid repeated freeze-thaw cycles.
Detection Antibody: Store at 4°C and protect it from prolonged exposure to light for up to 6 months from date of receipt. Do not freeze!
Standard: Store lyophilized standard at -20°C to -80°C for up to 6 months from date of receipt. Aliquot and store the reconstituted standard at -80°C for up to 1 month. Avoid repeated freezethaw cycles.

Sensitivity

The minimum detectable dose of Influenza B HA was determined to be approximately 62.5 pg/ml.
This is defined as at least three times standard deviations above the mean optical density of 10 replicates of the zero standard.

General Description

The influenza viral Hemagglutinin (HA) protein is a homo trimer with a receptor binding pocket on the globular head of each monomer. HA has at least 18 different antigens. These subtypes are named H1 through H18.HA has two functions. Firstly, it allows the recognition of target vertebrate cells, accomplished through the binding to these cells' sialic acid-containing receptors. Secondly, once bound it facilitates the entry of the viral genome into the target cells by causing the fusion of host endosomal membrane with the viral membrane. The influenza virus Hemagglutinin (HA) protein is translated in cells as a single protein, HA0, or hemagglutinin precursor protein. For viral activation, hemagglutinin precursor protein (HA0) must be cleaved by a trypsin-like serine endoprotease at a specific site, normally coded for by a single basic amino acid (usually arginine) between the HA1 and HA2 domains of the protein. After cleavage, the two disulfide-bonded protein domains produce the mature form of the protein subunits as a prerequisite for the conformational change necessary for fusion and hence viral infectivity

Standard Curve

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

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References

Variability in biological behaviour, pathogenicity, protectotype and induction of virus neutralizing antibodies by different vaccination programmes to infectious bronchitis virus genotype Q1 strains from Chile

AVIAN PATHOLOGY

Authors: de Wit, J. J.; Dijkman, R.; Guerrero, P.; Calvo, J.; Gonzalez, A.; Hidalgo, H.

Abstract

In the period from July 2008 to 2010, a disease episode resulting in serious economic losses in the major production area of the Chilean poultry industry was reported. These losses were associated with respiratory problems, increase of condemnations, drops in egg production and nephritis in breeders, laying hens and broilers due to infections with infectious bronchitis virus (IBV). Twenty-five IBV isolates were genotyped and four strains were selected for further testing by pathotyping and protectotyping. Twenty-four IBV isolates were of the Q1 genotype. The experiments also included comparing the ability of six vaccination programmes to induce virus neutralizing antibodies (VNA) in layers against four selected Chilean strains. Despite the high genetic homology in the S1 gene between the four strains, the heterogeneity in biological behaviour of these different Q1 strains was substantial. These differences were seen in embryonated eggs, in cell culture, in pathogenicity and in level of cross-protection by IBV Massachusetts (Mass) vaccination. This variability underlines the importance of testing more than one strain per serotype or genotype to determine the characteristics of a certain serotype of genotype. The combination of Mass and 793B vaccine provided a high level of protection to the respiratory tract and the kidney for each strain tested in the young birds. The combination of broad live priming using Mass and 793B vaccines and boosting with multiple inactivated IBV antigens induced the highest level of VNA against Q1 strains, which might be indicative for higher levels of protection against Q1 challenge in laying birds.

Viral interference between H9N2-low pathogenic avian influenza virus and avian infectious bronchitis virus vaccine strain H120 in vivo

COMPARATIVE IMMUNOLOGY MICROBIOLOGY AND INFECTIOUS DISEASES

Authors: Rim, Aouini; Nacira, Laamiri; Jihene, Nsiri; Said, Salhi; Khaled, Miled; Ahmed, Rejab; Abdeljelil, Ghram

Abstract

The interaction between a low pathogenic avian influenza virus (A/CK/TUN/145/2012), a H9N2 Tunisian isolate, and a vaccine strain (H120) of avian infectious bronchitis, administered simultaneously or sequentially three days apart to chicks during 20 days, was evaluated using ELISA antibody levels, quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analyses and histopathology examination. First, the in vivo replication interference of avian influenza virus (AIV) and infectious bronchitis virus (IBV) was evaluated using qRT-PCR to detect accurately either AIV or IBV genomes or viral copy numbers during dual infections. Second, we have determined the amount of specific antibodies in sera of chick's infected with AIV alone, IBV alone, mixed AIV + IBV, IBV then AIV or AIV IBV 3 days later using an ELISA test. Finally, histopathological analyses of internal organs from inoculated chicks were realized. Quantitative results of AIV and IBV co-infection showed that interferences between the two viruses yielded decreased viral growth. However, in the case of super-infection, the second virus, either AIV or IBV, induced a decrease in the growth of the first inoculated virus. According to our results, vaccine application was safe and do not interfere with AIV H9N2 infection, and does not enhance such infection. In conclusion, co-infection of chicks with AIV and IBV, simultaneously or sequentially, affected the clinical signs, the virus replication dynamics as well as the internal organ integrity. The results proposed that infection with heterologous virus may result in temporary competition for cell receptors or competent cells for replication, most likely interferon-mediated.