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Yellow fever virus

Yellow fever virus


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Yellow fever virus

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Viviana Popa, MD

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.

Now, from the skin, infected dendritic cells travel through lymphatic vessels to the lymph nodes, where the virus escapes into the bloodstream. From there, the infection spreads to various organs like the liver, kidneys, stomach, or the heart. The liver is usually the first target, so yellow fever is associated with hepatitis, or inflammation of the liver. The liver cells shrivel up and die, and they’re seen as Councilman bodies on histology. If the virus spreads to the kidneys, it causes renal tubular damage, resulting in renal failure. In the stomach, the virus can erode the gastric mucosa causing hemorrhage. If blood stays in the stomach for some time, the red blood cells are broken down by gastric acid, giving it a dark, coffee-ground like color. Finally, If the virus infects the heart, it can damage myocardial fibers, which can result in arrhythmias and myocardial infarction.

Yellow fever is an acute viral disease. In most cases, symptoms include fever, chills, loss of appetite, nausea, muscle pains particularly in the back, and headaches. Symptoms typically improve within five days. In some people within a day of improving, the fever comes back, abdominal pain occurs, and liver damage begins causing yellow skin. If this occurs, the risk of bleeding and kidney problems is also increased.