Chikungunya Virus Antibody (3E7b) - BSA Free

Immunocytochemistry/Immunofluorescence: Chikungunya virus Antibody (3E7b) [NBP2-53118] - Anti-CHIKV IgM (3E7b) and (8A2c) are used to stain chikungunya virus-infected cells. There is no staining observed in the mock infected cells. DAPI was used to stain the nucleus of the cells.

• Reactivity: V-Vi
• Applications: WB, ELISA, Func, ICC/IF, IHC
• Clone: 3E7b
• Clonality: Monoclonal
• Host: Mouse
• Conjugate: Unconjugated
• Format: BSA Free
• Concentration: 1 mg/ml

Chikungunya Virus Antibody (3E7b) - BSA Free Summary

• Immunogen: Live chikungunya virus
• Specificity: Both Anti-CHIKV [3E7b] and Anti-CHIKV [8A2c] bind strongly to native CHIKV surface and potently neutralize CHIKV replication.
• Isotype: IgM
• Clonality: Monoclonal
• Host: Mouse
• Purity: Thiophilic Chromatography

Applications/Dilutions

• Dilutions:
  • ELISA 1:100 - 1:2000
  • Functional
  • Immunocytochemistry/ Immunofluorescence 1:10-1:500
  • Immunohistochemistry 1:10 - 1:500
  • Western Blot 1:100 - 1:2000
• Application Notes: Both NBP2-53117 and NBP2-53118 bind strongly to native Chikungunya Virus surface and potently neutralize Chikungunya Virus replication. Positive control(s): Infected BHK cells

Reactivity Notes

Use in Virus reported in scientific literature (PMID:33806252).

Packaging, Storage & Formulations

• Storage: Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles.
• Buffer: PBS
• Preservative: 0.02% Sodium Azide
• Concentration: 1 mg/ml
• Purity: Thiophilic Chromatography

Alternate Names for Chikungunya Virus Antibody (3E7b) - BSA Free

• Chikungunya

Background

Chikungunya virus (CHIKV) belongs to the family of alphaviruses and is transmitted by Aedes mosquitoes resulting in infection characterized by symptoms including arthritis-like joint pain and inflammation, fever, rash, and headache (1-3). The CHIKV genome consists of an 11.8 kilobase (kb) positive-sense, single-stranded RNA virus that has two open reading frames (ORFs) (1-3). The first ORF at the 5' end encodes a 2472 amino acid (aa) nonstructural polyprotein and the ORF at the 3' end encodes a 1244 aa structural polyprotein (1-3). The polyproteins generate four nonstructural proteins (nsP1-4) and five structural proteins: capsid (C), envelope E1, E2, E3, and 6K (1-3). The nonstructural proteins comprise CHIKV's RNA replicase (1,2). Structurally, CHIKV has a diameter of ~65 nm and the virion is formed by an icosahedral nucleocapsid shell encapsulating genomic RNA and surrounded by a lipid bilayer envelope (2,3).

Although analysis suggests CHIKV originated in Africa over 500 years ago, first infections weren't reported until the 1950s (1-3). CHIKV has evolved three distinct genotypes, or strains, based on location, termed West African (WA), East/Central/Southern African (ECSA), and Asian (2-3). The WA strain has been most closely associated with enzootic transmission whereas the ECSA strain contributes more to urban epidemics (2). Nonhuman primates are the primary reservoir for the viral host with transmission occurring via mosquitos biting and infecting humans (1-3). Upon acute infection, the virus replicates in cells including fibroblasts and macrophages resulting in innate immune response in infected tissues characterized by infiltrating cells like macrophages, monocytes, natural killer (NK) cells, and lymphocytes (2,3). Infection results in increased production of proinflammatory cytokines such as interferon alpha (IFN-alpha) and interleukin 6 (IL-6), chemokines, and growth factors (2,3). Physical manifestations of infection are high fever, polyarthralgia, headache, arthritis, and rash (1-3). CHIKV symptoms can be confused with other infections like those from dengue fever and Zika virus (1-3). There are no specific antivirals or vaccines for CHIKV, but rather symptoms are treated with antipyretics and non-steroidal anti-inflammatory drugs (NSAIDs) (2,3). While in vitro culture models and in vivo rodent and non-human primate models have been used to study CHIKV pathogenesis and advance our knowledge of the disease, the specific cellular mechanisms are not fully understood (3).

References

1. Vu DM, Jungkind D, Angelle Desiree LaBeaud. Chikungunya Virus. Clin Lab Med. 2017;37(2):371-382. https://doi.org/10.1016/j.cll.2017.01.008

2. Silva LA, Dermody TS. Chikungunya virus: epidemiology, replication, disease mechanisms, and prospective intervention strategies. J Clin Invest. 2017;127(3):737-749. https://doi.org/10.1172/JCI84417

3. Ganesan VK, Duan B, Reid SP. Chikungunya Virus: Pathophysiology, Mechanism, and Modeling. Viruses. 2017;9(12):368. Published 2017 Dec 1. https://doi.org/10.3390/v9120368

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Publications for Chikungunya Virus Antibody (NBP2-53118)(2)

Publications using NBP2-53118

• SalomAo N, Brendolin M, Rabelo K et al. Spontaneous Abortion and Chikungunya Infection: Pathological Findings Viruses 2021-03-25 [PMID: 33806252] (IF/IHC, Virus)
• Schultz E, Jones T, Clamp H, Barr K Antibodies for Venezuelan Equine Encephalitis Virus Protect Embryoid Bodies from Chikungunya Virus Viruses 2020-03-04 [PMID: 32120905]