Yellow fever virus
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This page is about microbiologic aspects of the organism(s). For clinical aspects of the disease, see Yellow fever.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [2]
Overview
Yellow fever virus is caused by an arthropodborne virus of the Flaviviridae family in the genus Flavivirus. Flaviviruses are single stranded ribonucleic acid (RNA) viruses that replicate in the cytoplasm of infected cells. Seven genotypes of yellow fever virus have been identified, two in South America and five in Africa.
Yellow Fever Virus
Taxonomy
Viruses; ssRNA viruses; ssRNA positive-strand viruses, no DNA stage; Flaviviridae; Flavivirus; Yellow fever virus group [1]
Virus Characteristics
- Yellow fever is caused by the yellow fever virus, a 40- to 50-nm-wide enveloped RNA virus, the type species and namesake of the family Flaviviridae.
- It was the first illness shown to be transmissible by filtered human serum and transmitted by mosquitoes [2]
- The positive-sense, single-stranded RNA is around 11,000 nucleotides long and has a single open reading frame encoding a polyprotein. Host proteases cut this polyprotein into three structural (C, prM, E) and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5); the enumeration corresponds to the arrangement of the protein coding genes in the genome.[3]
- Yellow fever belongs to the group of hemorrhagic fevers.
- The viruses infect, amongst others, monocytes, macrophages, and dendritic cells.
- They attach to the cell surface via specific receptors and are taken up by an endosomal vesicle.
- Inside the endosome, the decreased pH induces the fusion of the endosomal membrane with the virus envelope.
- The capsid enters the cytosol, decays, and releases the genome. Receptor binding, as well as membrane fusion, are catalyzed by the protein E, which changes its conformation at low pH, causing a rearrangement of the 90 homodimer]]s to 60 homotrimers.
- After entering the host cell, the viral genome is replicated in the rough endoplasmic reticulum (ER) and in the so-called vesicle packets.
- At first, an immature form of the virus particle is produced inside the ER, whose M-protein is not yet cleaved to its mature form and is therefore denoted as prM (precursor M) and forms a complex with protein E.
- The immature particles are processed in the golgi apparatus by the host protein furin, which cleaves prM to M.
- This releases E from the complex which can now take its place in the mature, infectious virion.
References
- ↑ "NCBI Taxonomy Browser (Yellow Fever)".
- ↑ Staples JE, Monath TP (Aug 27, 2008). "Yellow fever: 100 years of discovery". JAMA : the Journal of the American Medical Association. 300 (8): 960–2. doi:10.1001/jama.300.8.960. PMID 18728272.
- ↑ Sampath A, Padmanabhan R (January 2009). "Molecular targets for flavivirus drug discovery". Antiviral Research. 81 (1): 6–15. doi:10.1016/j.antiviral.2008.08.004. PMC 2647018. PMID 18796313.