Human respiratory syncytial virus (RSV) (A2) Fusion glycoprotein / RSV-F ELISA Kit

Temporarily not available outside of China.The online Datasheet here is only a general version, for batch specific information please refer to the hard copy included in the product shipping package.
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Human respiratory syncytial virus (RSV) (A2) Fusion glycoprotein / RSV-F ELISA Kit: General Information

Product name
Human respiratory syncytial virus (RSV) (A2) Fusion glycoprotein / RSV-F ELISA Kit
Assay type
Solid Phase Sandwich ELISA (quantitative)
Conjugate
HRP
Sample type
Recombinant protein
Sensitivity
40.6 pg/mL
Assay range
93.75-6000 pg/mL
Specificity
Recognizes both recombinant and natural RSV RSV Fusion
Precision
  Intra-assay Precision
Sample 1 2 3
N 20 20 20
Mean(pg/mL) 1,025.35 2,148.77 4,219.00
SD 39.44 82.31 148.37
CV(%) 3.8% 3.8% 3.5%
  Inter-assay Precision
Sample 1 2 3
N 20 20 20
Mean(pg/mL) 1,455.52 2,793.43 4,629.42
SD 118.36 247.62 360.74
CV(%) 8.1% 8.9% 7.8%
Recovery
The recovery of RSV RSV-F spiked to different levels throughout the range of the assay in related matrices was evaluated.
Sample
supernatant (n=3)
Average % Recovery
103
Range
97-108%
Linearity
Supernatant
  Recovery of detected
1:2 100%
1:4 101%
1:8 99%
1:16 98%
Materials provided
1. 96 well microplate coated with Capture Antibody
2. Detection Antibody conjugated to HRP
3. Standards
4. Wash Buffer Concentrate
5. Dilution Buffer Concentrate
6. Color Reagent A
7. Color Reagent B
8. Stop Solution
Product overview
This Human respiratory syncytial virus (RSV) (A2) Fusion glycoprotein / RSV-F ELISA Kit is an enzyme-linked immunosorbent assay for the quantitative measurement of RSV RSV Fusion protein in Recombinant protein . It contains recombinant RSV RSV Fusion, and antibodies raised against the recombinant protein. This ELISA kit is complete and ready-to-use.
Shipping
This ELISA Kit is shipped at ambient temperature.
Storage
Unopened Kit: Store at 2 - 8℃
Opened/Reconstituted Reagents: Please refer to CoA

Human respiratory syncytial virus (RSV) (A2) Fusion glycoprotein / RSV-F ELISA Kit: Images

This standard curve is only for demonstration purposes. A standard curve should be generated for each assay.

Human respiratory syncytial virus (RSV) (A2) Fusion glycoprotein / RSV-F ELISA Kit: Synonyms

F ELISA Kit, RSV; HRSVgp08 ELISA Kit, RSV

RSV Fusion Background Information

Human respiratory syncytial virus (HRSV) is the most common etiological agent of acute lower respiratory tract disease in infants and can cause repeated infections throughout life. It is classified within the genus pneumovirus of the family paramyxoviridae. Like other members of the family, HRSV has two major surface glycoproteins (G and F) that play important roles in the initial stages of the infectious cycle. The G protein mediates attachment of the virus to cell surface receptors, while the F protein promotes fusion of the viral and cellular membranes, allowing entry of the virus ribonucleoprotein into the cell cytoplasm. The fusion (F) protein of RSV is synthesized as a nonfusogenic precursor protein (F), which during its migration to the cell surface is activated by cleavage into the disulfide-linked F1 and F2 subunits. This fusion is pH independent and occurs directly at the outer cell membrane, and the F2 subunit was identifed as the major determinant of RSV host cell specificity. The trimer of F1-F2 interacts with glycoprotein G at the virion surface. Upon binding of G to heparan sulfate, the hydrophobic fusion peptide is unmasked and induces the fusion between host cell and virion membranes. Notably, RSV fusion protein is unique in that it is able to interact directly with heparan sulfate and therefore is sufficient for virus infection. Furthermore, the fusion protein is also able to trigger p53-dependent apoptosis.
References
  • Martin-Gallardo A. et al., 1993, J Gen Virol. 74 (3): 453-8.
  • Jose A M. et al., 1997, J Gen Virol. 78: 2411-8.
  • Feldman SA. et al., 1999, J Virol. 73 (8): 6610-7.
  • Zlateva K.T. et al., 2004, J Virol. 78 (9): 4675-83.
  • Trento A. et al., 2006, J Virol. 80 (2): 975-84.
  • Branigan P J. et al., 2006, J Gen Virol. 87 (2): 395-8.
  • Eckardt-Michel J. et al., 2008, J. Virol. 82: 3236-49.
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