MOUSE ANTI-RIFT VALLEY FEVER VIRUS NUCLEOPROTEIN (M980)
Rift Valley Fever Nucleoprotein (M980) antibody recognises RVFV N protein and is suitable for use as in ELISA. This antibody can be used for detection when paired with MAB12335 which is used for capture.
PRODUCT DETAILS – MOUSE ANTI-RIFT VALLEY FEVER VIRUS NUCLEOPROTEIN (M980)
- Mouse anti Rift Valley Fever Nucleoprotein (M980). Recognises RVFV N protein in ELISA.
- Purified by Ion Exchange. >90% purity by SDS-PAGE.
- Presented in phosphate buffered saline, pH 7.2 with 0.05% sodium azide.
RVFV’s Nucleoprotein assembles to form a filamentous coat that protects RVFV’s RNA genome and is required for RNA replication and transcription by the viral polymerase. Ferron et al. produced a crystal structure of the protein, which shows that it forms a hexameric ring with structural flexibility to allow different RNA-binding conformations. Within the inner side of the ring, positive residues are shown to bind the RNA and are conserved across the Phlebovirus species. Xu et al. surmise that RVFV Nucleoprotein-subunit vaccines can induce cell-mediated response to protect against infection in mice and demonstrated that Nucleoprotein is a key immunogen during RVFV infection.
Rift Valley Fever was characterized in 1931 in the Rift Valley region of Kenya when it caused an outbreak among livestock. The causative agent – RVFV, is an enveloped RNA virus that belongs to the genus Phlebovirus, of the Bunyaviridae family. Bunyaviruses have tripartite genomes, consisting of small, medium and large RNA segments. The small, (S) segment is responsible for encoding the Bunyavirus Nucleoprotein, which in RVFV is responsible for ribonucleoprotein complexes that are essential for the RVFV life cycle and genome replication (Mottram et al., 2017).
RVFV is an arbovirus transmitted to domesticated livestock by the Aedes and Culex mosquitoes. Cattle, sheep, goats and camels are particularly susceptible to infection by RVFV and serve as amplifying hosts (WHO). The virus is currently found in sub-Saharan Africa, as well as in Egypt, Yemen, Saudi-Arabia, Madagascar and Mayotte. The continuing geographical expansion of RVFV is also cause for concern in Europe, where the virus is considered to be an emerging threat as recent outbreaks in the region have raised concerns that RVFV may spread to temperate climates through emerging, competent vectors.
Infection results in several syndromes that range from febrile illness to blindness, encephalitis and a lethal hemorrhagic fever. Vaccines that have been developed against RVFV are only partially attenuated, cost-prohibitive and only induce short-lived immunity. There are no drugs specifically available to treat RVFV infection and preventive efforts to avoid new outbreaks are mostly based on monitoring vector distribution
- Ferron et al. (2011). The Hexamer Structure of the Rift Valley Fever Virus Nucleoprotein Suggests a Mechanism for its Assembly into Ribonucleoprotein Complexes. Pathogens.
- Mottram et al. (2017). Mutational analysis of Rift Valley fever phlebovirus nucleocapsid protein indicates novel conserved, functional amino acids. Neglected Tropical Diseases.
- World health organisation (WHO). Rift Valley fever.
- Xu et al. (2013) The Nucleocapsid Protein of Rift Valley Fever Virus Is a Potent Human CD8 T Cell Antigen and Elicits Memory Responses. PLoS ONE 8(3).