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Yellow fever - Causes and pathogenesis
Last reviewed: 06.07.2025
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Causes of Yellow Fever
Yellow fever is caused by the RNA-containing virus Viceronhilus tropicus of the genus Flavivirus of the family Flaviviridae, which belongs to the group of arboviruses. The capsid has a spherical shape; the size is about 40 nm. It is unstable in the environment: it is quickly inactivated at low pH values, exposure to high temperatures and conventional disinfectants. It is preserved for a long time at low temperatures (in liquid nitrogen for up to 12 years). Antigenic relationship with dengue and Japanese encephalitis viruses has been established. The yellow fever virus agglutinates goose erythrocytes, causing a cytopathic effect in Hela, KB, Detroit-6 cells.
Yellow fever virus is cultured in chicken embryos and in cell cultures of warm-blooded animals. It is also possible to use cells of some arthropods, in particular the Aedes aegypti mosquito.
It has been shown that with long passages in cell culture and chicken embryos, the pathogenicity of the virus for monkeys is significantly reduced, which is used to prepare vaccines.
[ Pathogenesis of yellow fever
Yellow fever is transmitted by the bite of an infected mosquito. When infected, the virus penetrates the regional lymph nodes through the lymphatic vessels, where it replicates during the incubation period. After several days, it enters the bloodstream and spreads throughout the body. The duration of the viremia period is 3-6 days. During this time, the virus mainly enters the vascular endothelium, liver, kidneys, spleen, bone marrow and brain. As the disease develops, a pronounced tropism of the pathogen to the circulatory system of these organs is revealed. As a result, increased vascular permeability occurs, especially capillaries, precapillaries and venules. Dystrophy and necrosis of hepatocytes, damage to the glomerular and tubular systems of the kidneys develop. The development of thrombohemorrhagic syndrome is caused by both vascular damage and microcirculatory disorders, as well as a violation of the synthesis of plasma hemostasis factors in the liver.
The skin of deceased people is usually yellow, often purple due to venous hyperemia. Hemorrhagic rash is found on the skin and mucous membranes. Degenerative changes in the liver, kidneys, and heart are characteristic. The liver and kidneys are significantly enlarged, with small-point hemorrhages. fatty degeneration, foci of necrosis (in severe cases, subtotal). Characteristic changes are found in the liver, with Councilman bodies detected. In addition to changes in the cytoplasm, acidophilic inclusions (Torres bodies) are found in the nuclei of liver cells. They arise due to the proliferation of the virus in the cells and changes in their nuclei. Despite significant changes in the liver, after recovery, restoration of its functions is observed without the development of cirrhosis.
In some cases, the cause of death is kidney damage, characterized by swelling and fatty degeneration of the renal tubules up to necrosis. Colloid masses and blood casts accumulate in the tubules. Changes in the glomeruli of the kidneys are often insignificant. The spleen is filled with blood, the reticular cells of the follicles are hyperplastic. Degenerative changes occur in the heart muscle; hemorrhages are detected in the pericardium. Yellow fever is characterized by multiple hemorrhages in the stomach, intestine, lungs, pleura, as well as perivascular infiltrates in the brain.