Yellow Fever Virus Antibodies, Proteins & ELISA Kits

Non-human primates (NHPs) are reservoirs of YFV and mosquitos in these forested areas bite people who are visiting the location. These YFV infected individuals can carry the virus back to an urbanized setting and infect mosquitos in these regions. Aedes aegypti species are the main vector for transmission in urban locations and Haemagogus and Sabethes species are common vectors for YFV transmission in wild habitats. The symptoms experienced by YFV infected individuals are fever, vomiting and abdominal pain and they can further progress to both hepatic and renal failure. As well as this, jaundice occurs in 20% of the individuals experiencing YFV symptoms. There is currently a live attenuated vaccine for YFV which is highly effective but there are still outbreaks occurring in new regions of the world where there are vulnerable people.

YFV is composed of structural proteins such as capsid (C) proteins, envelope (E) proteins, pre-membrane (prM) proteins and membrane (M) proteins. YFV also has nonstructural components which are NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5. PrM is responsible for preventing premature fusion of the E protein to the cell surface during viral exocytosis. PrM is cleaved into M protein which is responsible for causing E protein to rearrange and promote pathogenesis through cell binding, virion assembly and immunogenicity. The E protein in YFV binds to host receptors such as transmembrane immunoglobulin and mucin domain-1 (TIM-1) and TIM-4.

Immunometabolism is an important area of science which encompasses regions of metabolism and immunology. Studies analyzing differentially expressed genes between symptomatic and asymptomatic YFV individuals identified that genes which were involved in The Citric Acid (TCA) cycle were reduced in symptomatic individuals. Reduced TCA cycle metabolism is associated with maladaptive ER stress which is seen when YFV synthesizes new macromolecules. This anabolic demand by viruses like YFV can cause the normal homeostatic balance in cells to tip to the production of Reactive Oxygen Species (ROS) which is associated with ER stress and inflammation. In comparison, it was found that reduced levels of ER stress and an increase in TCA cycle dependency for energy allows cells to cope with YFV metabolic demands and these individuals remain asymptomatic.

The clearance of YFV by the immune system has been shown to exacerbate the pathogenesis of the virus in some cases. There is an increase in cytokine and chemokine levels in YFV infected individuals in comparison to uninfected individuals and they include interleukin-6 (IL-6), IL-1beta, IL-1 receptor antagonist, tumor necrosis factor-alpha (TNF-alpha), IL-10, IL-8, Interferon (IFN), RANTES (CCL5), MIP-1alpha (CCL3), and MIP-1beta (CCL4). When YFV infects cells in the body there is an increase in the expression of CXCL10 (IP-10) which can promote trafficking of leukocytes to YFV infected sites. As well as this, src-kinase regulatory phosphatase (PTPRE) is reduced when YFV infects T cells in the body and it has been shown to impair T cell signaling.

Animal models are useful research tools which are often used in early stages of therapeutic product development and pathogenesis studies. The Syrian hamster model is a suitable model for studying YFV infections and the immune response elicited is the same as in humans whereby IFN-gamma and TNF-alpha are increased in the heart, spleen and kidney. NHPs are of particular interest for YFV research due to the fact that they are reservoirs for the disease.

YFV, West Nile Virus, Zika virus, Tick-borne encephalitis, Dengue and Japanese encephalitis belong to the genus Flavivirus. Many studies have identified structural and genetic similarities between the Flavivirus viruses. Studying components of these global health threats can aid in YFV therapeutic and vaccine research.

• Zika Virus
• West Nile Virus
• Japanese encephalitis