West Nile Virus Antibodies, Proteins & ELISA Kits

West Nile Virus (WNV) belongs to the genus Flavivirus and it is classified as a zoonotic arbovirus which is transmitted to humans, dogs, horses and many other mammals by mosquitos bites. A febrile illness is observed in WNV cases and 1 in 200 infected individuals develop a neuroinvasive disease which can lead to encephalitis, meningitis and mortality.

The Culex species is the most common vector of transmission for WNV and birds have been found to be the main host for both allowing viral amplification and harboring the virus. WNV was originally observed in Africa and then travelled to areas such as Europe, Asia and North America in the 1990s. WNV can now be found throughout most regions of the world and there is still currently no approved treatments or vaccines for WNV in humans.

WNV polyprotein is cleaved by both viral and host proteases into three structural components which are the capsid, envelope (E) and premembane (prM) proteins and seven nonstructural components called NS1, NS2A, NS2B, NS3, NS4A, NS4B and NS5. The envelope protein binds to receptors on host cells such as DC-SIGN, mannose and glycosaminoglycans and it is used for viral entry into the host. The prM protein prevents premature fusion of the E protein to the cell surface during viral exocytosis.

Biomarkers are useful tools for diagnostic and prognostic purposes. For WNV there are a variety of components which are either elevated or depleted in comparison to individuals who are not infected. A biomarker of particular interest that is elevated is the defensin-1 alpha (DEFA1) protein which is known for having antiviral effects.

WNV is able to rearrange host cell lipid metabolism whereby the virus is able to promote the synthesis of certain cellular lipids like fatty acids, cholesterol, sphingolipids and glycerophospholipids. There have been links with sphingolipid metabolism and Flavivirus biogenesis. Studies have also shown that when you block fatty acid synthase (FASN) there is reduced WNV replication observed. This can potentially be an antiviral strategy to pharmacologically manipulate the cellular lipids in order to reduce viral replication.

Understanding immunopathogenesis in the central nervous system (CNS) could help with the development of therapies for WNV whereby individuals could use knowledge with anti-inflammatory agents in order to minimize neuronal damage observed in WNV infections.

There is an increase in cytokine and chemokine levels in WNV infected individuals in comparison to uninfected individuals and they include interleukin-6 (IL-6), IL-1beta, tumor necrosis factor-alpha (TNF-alpha), IL-10, IL-2, IL-8, Interferon (IFN), MIP-1alpha (CCL3), and MIP-1beta (CCL4). When WNV infects neurons in the body there is an increase in the expression of CXCL10 (IP-10) which can promote trafficking of CD8⁺T cells specific for WNV. Since there is also an increased expression of MIP-1alpha and MIP-1beta there is an increase in CCR5 dependent trafficking of CD8⁺ T cells, CD4⁺ T cells and macrophages. When there is a mutation of CCR5, there is an increase in viral replication. There have also been studies performed whereby CXCR4 antagonists can increase CD8⁺ T cell trafficking to the CNS in WNV infections. Interferon-inducible transmembrane protein (IFITM) has been shown to inhibit the early stages of WNV replication.

The use of animal models are important for early phase studies of therapeutic therapies and for gathering data on how a virus such as WNV affects the body. For example, Syrian hamsters have been shown to be a suitable model for WNV whereby it models the pathogenesis of the virus and the progression of neurological defects it implements. As well as this, Syrian hamster model studies have shown how immunosuppressed models mirror WNV in cancer patients.

WNV, Yellow fever, Zika virus, Tick-borne encephalitis, Dengue and Japanese encephalitis belong to the genus Flavivirus. Many studies have identified structural similarities between the Flavivirus viruses and it was discovered that WNV shares an amino acid sequence identity similarity of 57.0% with Zika virus. Studying components of these viruses which have a similar pathogenesis, can aid in WNV vaccine and therapeutic research.

• Zika Virus
• Yellow Fever
• Japanese encephalitis