Johns Hopkins ABX Guide
Yellow fever virus
MICROBIOLOGY
- Yellow fever virus (YFV) is the prototype member of the approximately 75 viruses of the Flaviviridae family; "flavus" derives from the Latin word for yellow.
- Mosquito vector
- YFV was first isolated in 1927.
- There is 1 serotype with 7 distinct genotypes.
- South America: 2 genotypes
- Africa: 5 genotypes
- Single-stranded RNA virus with an 11 kilobase genome composed of 3 parts:[9]
- 5’ non-coding region
- A single open reading frame (ORF) that 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 clathrin-dependent endocytosis
- Non-Structural (NS): NS1, NA2a, NS2b, NS3, NS4a, NS4b, and NS5 are involved in:
- RNA replication
- Post-translational cleavage of the viral polyprotein
- Structural
- 3’ non-coding region
- Cell targets
- The virus is introduced by blood-feeding mosquitoes into the epidermis, where resident dendritic cells (DCs) are the principal target for early virus replication.[10]
- 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.
- The virus is introduced by blood-feeding mosquitoes into the epidermis, where resident dendritic cells (DCs) are the principal target for early virus replication.[10]
- Immune evasion[9]
- 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[9] 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.
- Pro-inflammatory mediators are significantly higher in patients with fatal illness when compared with survivors[9] including:
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Last updated: May 10, 2021
Citation
Hynes, Noreen A. "Yellow Fever Virus." Johns Hopkins ABX Guide, The Johns Hopkins University, 2021. 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; 2021. https://peds.unboundmedicine.com/pedscentral/view/Johns_Hopkins_ABX_Guide/540672/all/Yellow_fever_virus. Accessed November 29, 2023.
Hynes, N. A. (2021). Yellow fever virus. In Johns Hopkins ABX Guide. The Johns Hopkins University. 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; 2021. [cited 2023 November 29]. 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
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Y1 - 2021/05/10/
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UR - https://peds.unboundmedicine.com/pedscentral/view/Johns_Hopkins_ABX_Guide/540672/all/Yellow_fever_virus
PB - The Johns Hopkins University
DB - Pediatrics Central
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