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| Recall that the YFV can only be spread to humans via a vector and not through any direct human-human or human-animal interaction. The virus enters the human body during a mosquito bite when the blood from an infected individual on the mouth of the mosquito enters into the blood stream of a non-affected individual. | Recall that the YFV can only be spread to humans via a vector and not through any direct human-human or human-animal interaction. The virus enters the human body during a mosquito bite when the blood from an infected individual on the mouth of the mosquito enters into the blood stream of a non-affected individual. | ||
| - | Once the YFV enters the bloodstream it is able to infect those cells that its E proteins are able to preferentially bind to. These susceptible cells are monocytes (Macrophages and / or Dendritic Cells). Once the E-proteins on the YFV binds to the receptors on these monocytes the virus is able to enter the cell via Receptor Mediated Phagocytosis. Once it enters the cell an endosome forms around the entered virus where H+ enters the endosome raising the pH of the endosome-virus vesicle. This increase in pH allows the viral RNA to be released. This viral RNA attaches onto the Rough Endoplasmic Reticulum of the cell where it begins to replicate in "sacs". In order to replicate it utilizes the host's own RNA-dependent-RNA-polymerase to initiate the replication by switching the positive strand to negative strand and allowing replication to proceed. | + | Once the YFV enters the bloodstream it is able to infect those cells that its E proteins are able to preferentially bind to. These susceptible cells are monocytes (Macrophages and / or Dendritic Cells) (Pulendran, 2009). Once the E-proteins on the YFV binds to the receptors on these monocytes the virus is able to enter the cell via Receptor Mediated Phagocytosis. Once it enters the cell an endosome forms around the entered virus where H+ enters the endosome raising the pH of the endosome-virus vesicle (Pulendran, 2009). This increase in pH allows the viral RNA to be released. This viral RNA attaches onto the Rough Endoplasmic Reticulum of the cell where it begins to replicate in "sacs". In order to replicate it utilizes the host's own RNA-dependent-RNA-polymerase to initiate the replication by switching the positive strand to negative strand and allowing replication to proceed (Pulendran, 2009). |
| - | Following replication, immature viral particles enter the Golgi network through vesicles in which the viral particles mature. Maturation simply implies that the viral RNA takes its icosahedron shape and the E proteins on the outer layer of the virion form a dimer. Once they have matured, hte vesicles with progeny virion are released into outer environment as the vesicle fuses with the cellular membrane. The above process is outlined in the diagram below: | + | Following replication, immature viral particles enter the Golgi network through vesicles in which the viral particles mature. Maturation simply implies that the viral RNA takes its icosahedron shape and the E proteins on the outer layer of the virion form a dimer. Once they have matured, the vesicles with progeny virion are released into outer environment as the vesicle fuses with the cellular membrane (Pulendran, 2009). The above process is outlined in the diagram below: |
| {{:yf_-_viral_replication.jpg|}} | {{:yf_-_viral_replication.jpg|}} | ||
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| 15. WHO (2014, March 1). Yellow Fever. Retrieved from http://www.who.int/mediacentre/factsheets/fs100/en/ | 15. WHO (2014, March 1). Yellow Fever. Retrieved from http://www.who.int/mediacentre/factsheets/fs100/en/ | ||
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| - | 10. Volk, D.E., May, F.J., Gandham, S.H., Anderson, A., Von Lindern, J.J., Beasley, D.W., Barrett, A.D., & Goreinstein, D.G. (2009). Structure of Yellow Fever Virus Envelope Protein Domain III. //US National Library of Medicine//, 394(1), 12-18. | ||
