Yellow fever virus

Yellow fever virus causes a disease called yellow fever, named so because severe forms of the disease result in jaundice, which is a yellowish pigmentation of the skin and mucous membranes. Yellow fever virus belongs to the flaviviridae family of viruses, which also includes dengue fever virus and Zika virus. Interestingly, the flaviviridae family is actually named after the yellow fever virus, flavus being Latin for yellow. The virus is endemic to regions of Africa and South America.

Yellow fever virus is an enveloped virus with an icosahedral capsid, which is a spherical protein shell made up of 20 equilateral triangular faces. Inside the capsid there’s a single-stranded, positive-sense ribonucleic acid, or RNA. This means that their RNA is actually mRNA, which can directly be translated by the host cell ribosomes into new copies of the viral proteins, which get assembled into new viruses.

Yellow fever virus doesn’t just affect humans, but also other primates like monkeys and apes. And it’s also considered an arbovirus because it’s transmitted via certain arthropod vectors, or carriers, specifically mosquitoes in the Haemagogus and Aedes genera. Haemogogus mosquitoes transmit the virus among monkeys in the jungle, and that’s called the Sylvatic cycle. If an unsuspecting person on a trek chances upon one of these mosquitoes in the jungle, then they get infected too, and end up spreading the virus to other people. Aedes mosquitoes, most commonly Aedes aegypti, transmit the virus in urban areas, and that’s called the urban cycle.

Alright, so when a mosquito bites you, it releases the yellow fever virus in between your skin cells. The virus especially targets dendritic cells, which are specialized immune cells that normally eat up, or phagocytose, antigens in the skin and transfer them to immune cells in the lymph nodes. The virus then latches onto specific receptors on the dendritic cell membrane, which allows the virus to be endocytosed, or engulfed, into cells. During endocytosis, the icosahedral capsid breaks open, allowing the viral RNA to gain access to the host cell cytoplasm. In the cytoplasm, the viral RNA hijacks the host cell ribosomes, which start making viral proteins, that are later assembled into new viruses. The newly made viruses leave the cell intact by exocytosis, which is like reverse endocytosis.