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    Yellow fever virus

    Noreen A. Hynes, M.D., M.P.H., D.T.M.&H.
    Yellow fever virus is a topic covered in the Johns Hopkins ABX Guide.

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    MICROBIOLOGY

    • Yellow fever virus (YFV) is the prototype member of the approximately 75 viruses of Flaviviridae family; "flavus" derives from the Latin word for yellow.
      • Mosquito vector
      • YFV first isolated in 1927.
    • There is 1 serotype with 7 distinct genotypes.[7]
      • South America: 2 genotypes
      • Africa: 5 genotypes
    • Single-stranded RNA virus with an 11 kilobase genome composed of 3 parts:[2]
      • 5’ non-coding region
      • a single open reading frame (ORF) which encodes 3 structural and 7 non-structural proteins
        • Structural
          • Capsid (C)
          • Membrane (prM)
          • Envelope (E): This is the main structural protein
            • Mediates virus entry into the cell via clarathrin-dependent endocytosis
        • Non-Structural (NS): NS1, NA2a, NS2b, NS3, NS4a, NS4b, and NS5 are involved in:
          • RNA replication
          • Post-translational clevage of the viral polyprotein
      • 3’ non-coding region
    • Cell targets
      • Virus introduced by blood-feeding mosquito into the epidermis where resident dendritic cells (DC) are the principle target for early virus replication.[3]
        • Toll-like receptors (TLRs) on the surface of DC are key in the critical role of sensing microbial stimuli.
        • DCs initiate and modulate the adaptive immune system.
      • DCs carry the virus via lymphatics to draining lymph nodes and subsequently to the bloodstream with eventual dissemination to cells in the liver, spleen, remaining lymph nodes, kidneys and heart.[7]
    • Immune evasion[2]
      • Inhibition of the innate interferon type I response is key
      • Non-human primate studies have demonstrated down-regulation of 43 genes associated with innate immunity, including
        • Interferon gamma receptor-1
        • CD83, a marker of DC maturation
        • TNFSF11: though to induce DCs to stimulate naive T cell proliferation
    • Inflammation
      • Pro-inflammatory mediators are significantly higher in patients with fatal illness when compared with survivors[2] including:
        • Tumor necrosis factor-alpha (TNF-α)
        • Interleukin-6 (IL-6)
        • Interleukin-1 receptor antagonist (IL-1RA)
        • Interferon-gamma inducible protein 10 (IP-10)
        • Monocyte chemoattractant protein-1 (MCP-1)
      • Similar findings were seen in rhesus macaques, the animal model for studying many aspects of yellow fever virus infection

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    Last updated: September 25, 2016

    Citation

    Hynes, Noreen A. "Yellow Fever Virus." Johns Hopkins ABX Guide, The Johns Hopkins University, 2016. Pediatrics Central, peds.unboundmedicine.com/pedscentral/view/Johns_Hopkins_ABX_Guide/540672/all/Yellow_fever_virus.
    Hynes NA. Yellow fever virus. Johns Hopkins ABX Guide. The Johns Hopkins University; 2016. https://peds.unboundmedicine.com/pedscentral/view/Johns_Hopkins_ABX_Guide/540672/all/Yellow_fever_virus. Accessed April 21, 2019.
    Hynes, N. A. (2016). Yellow fever virus. In Johns Hopkins ABX Guide. Available from https://peds.unboundmedicine.com/pedscentral/view/Johns_Hopkins_ABX_Guide/540672/all/Yellow_fever_virus
    Hynes NA. Yellow Fever Virus [Internet]. In: Johns Hopkins ABX Guide. The Johns Hopkins University; 2016. [cited 2019 April 21]. Available from: https://peds.unboundmedicine.com/pedscentral/view/Johns_Hopkins_ABX_Guide/540672/all/Yellow_fever_virus.
    * Article titles in AMA citation format should be in sentence-case
    TY - ELEC T1 - Yellow fever virus ID - 540672 A1 - Hynes,Noreen,M.D., M.P.H., D.T.M.&H. Y1 - 2016/09/25/ BT - Johns Hopkins ABX Guide UR - https://peds.unboundmedicine.com/pedscentral/view/Johns_Hopkins_ABX_Guide/540672/all/Yellow_fever_virus PB - The Johns Hopkins University DB - Pediatrics Central DP - Unbound Medicine ER -