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Yellow Fever

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Yellow fever is a viral hemorrhagic disease caused by a flavivirus transmitted by infected Aedes or Haemagogus mosquitoes.

After a mosquito bite, the virus enters the skin and infects local immune cells. These cells carry the virus to nearby lymph nodes, where the virus multiplies and buds off.

Viral particles then enter the bloodstream—a process known as viremia—and spread to various organs, such as the liver.

In the liver, the virus infects hepatocytes, causing apoptosis.

Kupffer cells, the liver’s macrophages, release cytokines that intensify inflammation and tissue damage.

This damage disrupts bilirubin metabolism, causing it to build up in the liver and then in the blood.

Excess bilirubin leads to jaundice—the yellowing of the skin and eyes that gives the disease its name.

Yellow fever progresses in three phases: a febrile stage with fever and pain, a short remission phase, and a toxic phase with bleeding, jaundice, and organ failure.

Overview

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Yellow fever is a viral hemorrhagic disease caused by the yellow fever virus (YFV), a member of the Flaviviridae family. It is transmitted primarily by Aedes and Haemagogus mosquitoes in tropical and subtropical regions of Africa and South America. After transmission through a mosquito bite, the virus initially replicates in skin-resident immune cells such as dendritic cells and macrophages. These cells then migrate to the lymph nodes, where viral replication increases, eventually leading to viremia. This systemic spread allows the virus to reach vital organs, particularly the liver.

Hepatic Pathogenesis

The liver is a primary site of YFV replication. The virus infects hepatocytes, causing both apoptosis and necrosis. At the same time, Kupffer cells—the liver’s specialized macrophages—worsen the damage by releasing proinflammatory cytokines. This immune-mediated injury intensifies hepatocellular damage beyond the direct effects of the virus. The destruction of hepatocytes disrupts bilirubin metabolism, resulting in hyperbilirubinemia. The buildup of bilirubin in tissues presents clinically as jaundice, a key feature of severe yellow fever.

Clinical Course

The disease usually progresses through three stages. The initial febrile phase includes fever, myalgia, and headache. This may be followed by a brief remission during which symptoms temporarily improve. In severe cases, the illness advances to a toxic phase, characterized by hemorrhage, jaundice, renal dysfunction, and multi-organ failure. Mortality can be high at this stage, making prevention critical. It is also important to note that many infected individuals remain asymptomatic or experience only mild symptoms.

Immunity and Prevention

A single dose of the live-attenuated viral vaccine provides long-lasting immunity and is the cornerstone of prevention. The vaccine triggers strong neutralizing antibody responses that protect against future infections. Vector control and broad vaccination coverage are essential public health strategies for reducing transmission in endemic regions.

Transcript

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Yellow Fever Virus

Viral Hemorrhagic Disease

Flaviviridae Family

Aedes Mosquitoes

Haemagogus Mosquitoes

Hepatic Pathogenesis

Hepatocyte Infection

Hyperbilirubinemia