Mouse Monoclonal RSV antibody. Suitable for ELISA and reacts with Respiratory syncytial virus samples.
Preservative: 0.09% Sodium azide
Constituents: PBS
| ELISA | |
|---|---|
| Respiratory syncytial virus | Expected |
| Species | Dilution info | Notes |
|---|---|---|
Species Respiratory syncytial virus | Dilution info Use at an assay dependent concentration. | Notes - |
Respiratory syncytial virus
Mouse Monoclonal RSV antibody. Suitable for ELISA and reacts with Respiratory syncytial virus samples.
Preservative: 0.09% Sodium azide
Constituents: PBS
F protein of Respiratory Syncytial Virus. Reactive with surface domain of both mature RSV virions and virion envelopes without formed inner nucleocapsid structures. Does not react with Influenza A (H1N1), Influenza A (H3N2), Influenza B, Parainfluenza 1, 2, 3 and Adenovirus.
>90% pure (SDS-PAGE) Sourced from tissue culture supernatant.
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The Respiratory Syncytial Virus (RSV) is a single-stranded RNA virus with a mass of approximately 15000 kDa. It primarily infects the epithelial cells in the respiratory tract. RSV is well-studied due to its ability to fuse with host cells facilitating the entry of its nucleocapsid into the cytoplasm. This fusion process involves the RSV F protein an important virulence factor which triggers membrane fusion at neutral pH. The G protein of RSV which attaches to host cells is also important for its infectivity and cell entry aiding its transmission and pathogenicity.
The virus is a significant pathogen in infants and the elderly causing respiratory illnesses. It is a part of the Pneumoviridae family and is known for inducing strong inflammatory responses in the lower respiratory tract. During infection RSV manipulates host cellular mechanisms such as the innate immune response to proliferate. It is not a part of a complex but interacts with host cell receptors through the G protein which attaches the virus to the host initiating a cascade of cellular interactions critical for infection.
RSV disrupts typical immune signaling particularly interfering with the toll-like receptor (TLR) signaling pathway. This alteration allows the virus to evade the host's innate immune system. Additionally the RSV infection modulates the NF-kB pathway which plays a role in inflammation and immune regulation. RSV's interaction with these pathways can influence cytokine production and inflammatory responses with impacts on related proteins like TLRs and NF-kB inhibitors.
RSV is a major cause of bronchiolitis and pneumonia in young children and can exacerbate asthma and chronic obstructive pulmonary disease (COPD) in adults. The infection often leads to severe respiratory symptoms which result from the immune response to the virus. RSV’s connection with diseases relates to proteins such as interleukins and other pro-inflammatory cytokines which can be significantly elevated during severe infections. Understanding these connections offers potential pathways for therapeutic interventions.
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This species and application combination has not been tested, but we predict it will work based on strong homology. However, this combination is not covered by our product promise.
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