What is Yellow Fever?

Yellow fever is a disease caused by infection with the yellow fever virus. The virus is a 40 to 50 nm enveloped RNA virus with positive sense of the family, Flaviviridae.

The virus is transmitted by the bite of mosquitos (the yellow fever mosquito, ''Aedes aegypti'', and other species) and is found in tropical and subtropical areas in South America and Africa, but not in Asia. The only known hosts of the virus are primates and several species of mosquito. The origin of the disease is most likely to be Africa, from where it was introduced to South America through the slave trade in the 16th century. Since the 17th century, several major epidemics of the disease have been recorded in the Americas, Africa and Europe. In the 19th century, yellow fever was deemed one of the most dangerous infectious diseases.

The disease presents itself in most cases with fever, nausea and pain and it disappears after several days. In some patients, a toxic phase follows, in which liver damage with jaundice (giving the name of the disease) can occur and lead to death. Because of the increased bleeding tendency (bleeding diathesis), yellow fever belongs to the group of hemorrhagic fevers. The WHO estimates that yellow fever causes 200,000 illnesses and 30,000 deaths every year in unvaccinated populations; around 90 % of the infections occur in Africa.

Yellow Fever symptoms

Yellow fever begins suddenly after an incubation period of three to six days. Most cases only cause a mild infection with fever, headache, chills, back pain, loss of appetite, nausea and vomiting. In these cases the infection lasts only three to four days. 15% of cases enter a second, toxic phase of the disease with recurring fever, this time accompanied by jaundice due to liver damage, as well as abdominal pain. Bleedings in the mouth, the eyes and in the gastrointestinal tract can cause vomitus containing blood (giving the name "vómito negro"). The toxic phase is fatal in approximately 20% of cases.

Surviving the infection causes life-long immunity and normally there are no remaining organ damages.

Yellow Fever Cause

Yellow fever is caused by the yellow fever virus, a 40 to 50 nm wide enveloped RNA virus belonging to the family Flaviviridae. The positive sense single-stranded RNA is approximately 11.000 nucleotides long and has a single open reading frame encoding a polyprotein. Host proteases cut this polyprotein into 3 structural (C, prM, E) and 7 non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5); the enumeration corresponds to the arrangement of the protein coding genes in the genome.

The viruses infect amongst others monocytes, macrophages and dendritic cells. They attach to the cell surface via specific receptors and are taken up by an endosomal vesicle. Inside the endosome, the decreased pH induces the fusion of the endosomal membrane with the virus envelope. Thus, the capsid reaches the cytosol, decays and releases the genome. Receptor binding as well as membrane fusion are catalyzed by the protein E, which changes its conformation at low pH, which causes a rearrangement of the 90 homodimers to 60 homotrimers.

There are three epidemiologically different infectious cycles,

When the disease takes a deadly course, a cardiovascular shock and multi organ failure with strongly increased cytokine levels (cytokine storm) follow. and lasts for at least 10 years (even 30 years later, 81 % of patients retained the immunity).

The attenuated live vaccine (stem 17D) was developed in 1937 by Max Theiler) mild, flu-like symptoms may develop.

In rare cases (less than one in 200,000 to 300,000 If the vaccination cannot be conducted for some reasons, dispensation is possible. In this case an exemption certificate issued by an WHO approved vaccination center is required.

Even though 32 of 44 countries where yellow fever occurs endemically do have vaccination programmes, in many of these countries fewer than 50% of their population is vaccinated.

Phylogenetic analysis identified seven genotypes of yellow fever viruses, and it is assumed that they are differently adapted to humans and to the vector ''A. aegypti''. Five genotypes occur solely in Africa, and is assumed that the West Africa-genotype I is especially virulent or infectious, because this type is often associated with major outbreaks of yellow fever. In South America two genotypes have been identified.

It is thought, that the virus originated in East or Central Africa and spread from there to West Africa. The virus as well as the vector ''A. aegypti'' were probably brought to South America by ship after 1492. The first probable outbreak of the disease was in 1648 in Yucatan, where the illness was termed ''xekik'' (black vomit). At least 25 major outbreaks followed, such as in Philadelphia 1793, where several thousand people died and the American administration as well as George Washington had to flee the city. Major outbreaks also occurred in Europe, e.g. in 1821 in Barcelona with several thousand victims. 1878, about 20,000 people died in an epidemic in the Mississippi River Valley and the last major outbreak in the US occurred in 1905 in New Orleans. Since the losses in the invasion of Cuba in the 1890s due to yellow fever were 13fold higher than the losses due to military operations, further experiments conducted by a team under Walter Reed successfully proved the ″Mosquito Hypothesis″. Yellow fever was thus the first virus shown to be transmitted by mosquitos. The physician William Gorgas then applied these insights and eradicated yellow fever from Havanna and fought yellow fever during the construction of the Panama Canal – after a French effort to build the canal had failed due, among other reasons, to the high incidence of yellow fever and malaria. Ribavirin treatment during the first five days after virus infection improved survival rates, reduced tissue damage in target organs (liver and spleen), prevented hepatocellular steatosis, and normalised alanine aminotransferase (a liver damage marker) levels. The results of this study suggest that ribavirin may be effective in the early treatment of yellow fever, and that its mechanism of action in reducing liver pathology in yellow fever virus infection may be similar to that observed with ribavirin in the treatment of hepatitis C, a virus related to yellow fever.

In the past, yellow fever has been researched by several countries as a potential biological weapon.


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