Yellow fever, the name conjures up images of people with jaundice and bleeding out of their orifices. This disease caused a number of epidemics during the 18th and 19th centuries, becoming a feared hemorrhagic disease (Monath, "Yellow Fever Virus" 1980). Yellow fever is an arthropod borne disease endemic to tropical South American, Central American and African countries, with high populations of mosquitoes. Transmission of the disease occurs in three areas: the savannah, jungle and urban locales (Monath, "Yellow Fever: an Update" 12). The disease cycles between humans or monkeys and Aedes aegypti mosquitoes each obtains the disease from the other (12). Although fear of the disease was prevalent during previous centuries now, the availability of vaccines and increased knowledge about the disease, allow for its management.
Yellow fever virus is an arthropod borne virus and part of the Flaviviridae family (Chastel). This Flavivirus is part of the Class IV Baltimore classification system, which indicates that it is a positive sense single stranded RNA virus (Monath, "Yellow Fever: an Update" 11). An icosahedral capsid and the envelope protect the genomic information, composed of about 10,000 nucleotides (Monath, "Yellow Fever Virus" 1980). Scientists detected only one serotype of the virus, but there are multiple strains and five genotypes (Monath, "Yellow Fever: an Update" 11).
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The envelope consists of an essential glycoprotein for the bacterial life cycle, E protein, this protein also encodes for the envelope. E protein provides yellow fever virus with a basis for attachment to a host cell (Monath, "Yellow Fever: an Update" 11). E protein attaches to a glycosaminoglycan receptor on the cell surface, such as heparin sulfate. After attachment, the virus enters the cell by receptor-mediated endocytosis and rids itself of its envelope via fusion (Monath, "Yellow Fever Virus" 1980). After entering the cell the positive sense single stranded RNA undergoes translation in order to produce the proteins necessary for production of viral offspring. Three of the proteins are structural, E protein, C protein, and prM protein, which code for the envelope, capsid, and a precursor to the capsid maturation protein, respectively (Monath, "Yellow Fever Virus" 1980). The other seven proteins are non-structural proteins, for example NS5 that encodes for the RNA polymerase necessary for the viral life cycle. Two of these non-structural proteins, NS1 and NS3, trigger immune system activity against the virus (Monath, "Yellow Fever: an Update" 11). NS1, specifically, will trigger an immune response because it is circulating in the blood of the infected individual (Monath, "Yellow Fever Virus" 1981).
Replication of the viral genome transpires after translation of the positive sense single stranded RNA, also (Monath, "Yellow Fever Virus" 1982). RNA replication of the Yellow Fever virus occurs by synthesis of a complementary negative sense single stranded RNA; the transcription of the negative sense single stranded RNA produces a product of positive sense single stranded RNA, used as the genomic information for the new viruses created (1982). Not all of the steps for assembly of the flavivirus are known (Patkar). The primary step of assembly takes place when the C protein and genome encounter each other forming the nucleocapsid. This step occurs without the necessity for interactions with the E protein and prM protein, which indicates that a non-structural protein mediates replication and assembly. Studies show that there is a possibility that the NS3 protein has a role in assembly of the virus particle (Patkar). In order for the virus to exit the cell it infected it steals the membrane from the endoplasmic reticulum and undergoes exocytosis (Monath, "Yellow Fever Virus" 1980).
Yellow fever virus has a life cycle that rotates from human or monkeys to mosquito. The virus enters the mosquito after the mosquito has bitten an infected individual. In the mosquito, the virus undergoes replication in the midgut and salivary glands in a temperature dependent manner, but does not affect the mosquito itself (Monath, "Yellow Fever Virus" 1984). The mosquito is a vector for the disease and transmits the disease to humans during bites. Most of the individuals bitten by carrier mosquitoes develop either abortive or subclinical infections, rather than the characteristic presentations of the disease (1985). After three to six days, the infected individual begins to show signs of the disease by displaying non-specific symptoms (1985). The initial symptoms the individual suffers will consist of a mild fever, chills, headaches, pain, and overall weakness; symptoms are similar to those of other diseases (CDC). During this period, any infected individual bitten by a mosquito will infect it with the yellow fever virus (Monath, "Yellow Fever Virus" 1985).
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After the initial symptoms, the individual may enter remission, and afterwards enter the toxic and hemorrhagic phase. These symptoms are the characteristic symptoms of the disease and include the following: high fever, pain, bloody vomit, bruising, nosebleeds, jaundice, and proteinuria (CDC). The immune system clears the virus out of the body by antibody neutralization and agglutination, in particular IgG (Monath, "Yellow Fever Virus" 1986). If the immune system does not remove the virus before irreversible damage occurs to the cells, the infected individual can enter coma, shock, or die (CDC).
How the virus affects human cells is unknown, but studies conducted on non-human primates shed some light (Monath, "Yellow Fever Virus" 1986). In these studies, the virus infects the liver and other organs, indicating viscerotropism. In the liver, the virus undergoes early virus replication in the macrophages of the liver, also known as Kupffer cells, triggering their necrosis (1986). Late in the infection, the virus invades the hepatocytes triggering cellular apoptosis and necrosis in the midzone of the liver (Monath, "Yellow Fever: an Update" 14). This viral infiltration causes the liver to swell and decreases the synthesis of clotting factors in the liver (Monath, "Yellow Fever Virus" 1986). The effects of the virus on the liver trigger the primary symptoms of jaundice and hemorrhaging. The virus infects and has effects on the spleen, kidney, lymph, and muscle cells of the heart, as well, which increases the symptoms displayed (1986).
Detection of the virus in the clinic occurs via antibody testing with enzyme-linked immunosorbant assays, ELISA, and immuno-fluorescence (Monath, "Yellow Fever Virus" 1986). If the infected individual is in an endemic area, training of doctors allows simple ways to detect the disease using clinical differentiation of similar diseases (Monath, "Yellow Fever: an Update" 15). Although detection of an infected individual is simple, no treatment is available for the person (WHO). The most doctors can do is provide the patients with supportive care for the fever or dehydration. Although fluid replacement is recommended to combat dehydration and blood loss, patients do not seem to respond readily to this treatment indicating the intensive damage to the patients internal organs (Monath, "Yellow Fever: an Update" 17). Since no treatment is available after infection occurs, prevention is the best bet to avert initial occurrence of yellow fever.
Prevention of the disease is the easiest way to avoid the disease. Since mosquitoes are the vector that spreads the disease, there are steps in place to eliminate breeding sites, but these have not been successful in the long run (Barnett). Individuals can also limit their exposure to mosquitoes by using mosquito repellents and wearing clothing that prevents mosquito bites (CDC).
The best form of prevention is in the form of vaccination (WHO). There are two vaccines available, 17D and Dakar FNV, both of which are live attenuated vaccines, cultured in eggs. The most widely used and effective vaccine is 17D, which also has the least adverse reactions (Monath, "Yellow Fever: an Update" 17-8). There are minimal risks, but in an unlucky few, the vaccine can promote severe side effects such as the following: neurological disease, allergic reactions, and yellow-fever associated viscerotropic disease (Barnett). These side effects are most likely due to the attenuation of the virus, since the virus is still alive and can cause some effects. Although there are risks associated with the vaccine, vaccination is highly recommended for individuals not including babies, pregnant women, and the severely immuno-compromised (WHO). Vaccination programs are in place, in areas where the disease is endemic; vaccination is required for entry to, or exit from endemic countries along with a record of the immunization (Monath, "Yellow Fever: an Update" 17).
Yellow Fever is primarily encountered in 45 countries spread throughout Latin America and Africa, especially tropical regions of these countries (WHO). Transmission of the disease increases during the rainy season, since mosquitoes breed in watery areas (Monath, "Yellow Fever Virus" 1985). During these periods, travelers should not enter endemic countries to limit exposure with infected mosquitoes. Cases most often occur in urban settings, or in male individuals with occupations that increase exposure to jungle mosquitoes (Chastel). Although minimal cases of the virus are around today, the virus is still prevalent in these areas and lack of information leads to unwarranted deaths of unvaccinated travelers.
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Overall, a Flavivirus transmitted via a mosquito vector causes Yellow Fever. Studies increase the knowledge on the virus particle proteins and there effects, as well as attempting discoveries on how the virus affects human cells. The knowledge gained allowed the development of a vaccine, and may allow development of some type of treatment for the disease. There are rare cases of this viral hemorrhagic disease, but the few cases often prove to be fatal. Although Yellow Fever virus does not cause epidemics on the scale of the 19th century, it is not extinct and is still prevalent in Latin American and African countries.