Yellow Fever Virus Recombinant
Yellow fever is an acute viral hemorrhagic disease caused by the yellow fever virus (YFV), which belongs to the genus Flavivirus within the family Flaviviridae . The disease is transmitted to humans primarily through the bites of infected Aedes and Haemagogus mosquitoes . Yellow fever is endemic in tropical regions of Africa and South America .
Key Biological Properties: Yellow fever virus is a small, enveloped virus with a positive-sense single-stranded RNA genome of approximately 11 kilobases . The genome encodes a single polyprotein that is processed into three structural proteins (capsid, membrane, and envelope) and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5) .
Expression Patterns and Tissue Distribution: The virus primarily targets liver cells, leading to hepatocellular damage and jaundice . It also affects other organs, including the kidneys and heart .
Primary Biological Functions: The yellow fever virus is responsible for causing yellow fever, which manifests in two phases: an acute phase with symptoms such as fever, muscle pain, and headache, and a toxic phase characterized by jaundice, bleeding, and multi-organ failure .
Role in Immune Responses and Pathogen Recognition: The immune response to yellow fever involves both innate and adaptive immunity. The E protein of the virus plays a crucial role in the induction of neutralizing antibodies and protective immunity .
Mechanisms with Other Molecules and Cells: Yellow fever virus enters host cells by binding to specific receptors on the cell surface, followed by endocytosis . Once inside the cell, the viral RNA is released and translated into viral proteins, which then assemble into new virions .
Binding Partners and Downstream Signaling Cascades: The envelope protein (E) is essential for viral entry and fusion with host cell membranes . The non-structural proteins, particularly NS3 and NS5, play critical roles in viral replication and immune evasion .
Regulatory Mechanisms Controlling Expression and Activity: The expression of yellow fever virus proteins is regulated at both the transcriptional and post-transcriptional levels . Post-translational modifications, such as glycosylation of the envelope protein, are crucial for viral infectivity and immune evasion .
Diagnostic Tools: Diagnostic methods for yellow fever include polymerase chain reaction (PCR) for detecting viral RNA and enzyme-linked immunosorbent assay (ELISA) for detecting antibodies .
Therapeutic Strategies: While there is no specific antiviral treatment for yellow fever, supportive care, including hydration and treatment of symptoms, is essential . Vaccination is the most effective preventive measure .
Role Throughout the Life Cycle: Yellow fever virus is maintained in a cycle between mosquitoes and vertebrate hosts, primarily non-human primates . Humans become infected when bitten by an infected mosquito. The virus can be transmitted in three cycles: jungle (sylvatic), intermediate (savannah), and urban . The urban cycle involves transmission between humans and urban mosquitoes, primarily Aedes aegypti .