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West Nile fever - Causes and pathogenesis
Last reviewed: 04.07.2025
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Causes of West Nile Fever
The cause of West Nile fever is the West Nile fever virus, which belongs to the Flavivirus genus of the Flaviviridae family. The genome is single-stranded RNA.
Replication of the virus occurs in the cytoplasm of affected cells. West Nile fever virus has a significant capacity for variability, which is due to the imperfection of the mechanism for copying genetic information. The greatest variability is characteristic of genes encoding envelope proteins responsible for the antigenic properties of the virus and its interaction with tissue cell membranes. West Nile fever virus strains isolated in different countries and in different years have no genetic similarity and have different virulence. The group of "old" West Nile fever strains, isolated mainly before 1990, is not associated with severe CNS lesions. The group of "new" strains (Israel-1998/New York-1999, Senegal-1993/Romania-1996/Kenya-1998/Volgograd-1999, Israel-2000) is associated with mass and severe human diseases.
[ Pathogenesis of West Nile fever
The pathogenesis of West Nile fever has been poorly studied. It is believed that the virus spreads hematogenously, causing damage to the vascular endothelium and microcirculatory disorders, and in some cases, the development of thrombohemorrhagic syndrome. It has been established that viremia is short-term and non-intensive. The leading factor in the pathogenesis of the disease is damage to the membranes and brain tissue, leading to the development of meningeal and general cerebral syndromes, focal symptoms. Death usually occurs on the 7th-28th day of the disease due to disruption of vital functions due to edema-swelling of the brain tissue with dislocation of stem structures, necrosis of neurocytes, and hemorrhages in the brain stem.
Autopsy reveals edema and plethora of the meninges, small focal perivascular hemorrhages, large hemorrhages (up to 3-4 cm in diameter). Enlargement of the cerebral ventricles, plethora of the choroid plexus, multiple foci of softening in the cerebral hemispheres, small-point hemorrhages in the bottom of the fourth ventricle, and dislocation of the brainstem in 30% of the deceased. Microscopic examination reveals vasculitis and perivasculitis of the meninges, focal encephalitis with the formation of mononuclear infiltrates. In the vessels of the brain, there is a picture of plethora and stasis, fibrinoid swelling and necrosis of the vascular wall. In the ganglion cells, there are pronounced dystrophic changes up to necrosis, pronounced perivascular and pericellular edema.
Significant changes are found in the heart: muscle laxity, stromal edema, myocyte dystrophy, areas of muscle fiber fragmentation and myolysis. Dystrophic changes are found in the kidneys. In some patients, signs of generalized thrombohemorrhagic syndrome are determined.
West Nile fever virus is detected by PCR in cerebrospinal fluid, brain tissue, kidneys, heart, and to a lesser extent in the spleen, lymph nodes, and liver.