Yellow Fever
Yellow fever is a viral disease of typically short duration. [3] In most cases, symptoms include fever, chills, loss of appetite, nausea, muscle pains – particularly in the back – and headaches.[3] Symptoms typically improve within five days.[3] In about 15% of people, within a day of improving the fever comes back, abdominal pain occurs, and liver damage begins causing yellow skin.[3][6] If this occurs, the risk of bleeding and kidney problems is increased.[3]
The disease is caused by yellow fever virus and is spread by the bite of an infected mosquito.[3] It infects only humans, other primates, and several types of mosquitoes.[3] In cities, it is spread primarily by Aedes aegypti, a type of mosquito found throughout the tropics and subtropics.[3] The virus is an RNA virus of the genus Flavivirus.[7] The disease may be difficult to tell apart from other illnesses, especially in the early stages.[3] To confirm a suspected case, blood-sample testing with polymerase chain reaction is required.[4]
A safe and effective vaccine against yellow fever exists, and some countries require vaccinations for travelers.[3] Other efforts to prevent infection include reducing the population of the transmitting mosquitoes.[3] In areas where yellow fever is common, early diagnosis of cases and immunization of large parts of the population are important to prevent outbreaks.[3] Once a person is infected, management is symptomatic; no specific measures are effective against the virus.[3] Death occurs in up to half of those who get severe disease.[3][8]
In 2013, yellow fever resulted in about 127,000 severe infections and 45,000 deaths worldwide,[3] with nearly 90 percent of these occurring in Africa.[4] Nearly a billion people live in an area of the world where the disease is common.[3] It is common in tropical areas of the continents of South America and Africa, but not in Asia.[3][9] Since the 1980s, the number of cases of yellow fever has been increasing.[3][10] This is believed to be due to fewer people being immune, more people living in cities, people moving frequently, and changing climate increasing the habitat for mosquitoes.[3]
The disease originated in Africa and spread to South America in the 17th century with the Spanish and Portuguese importation of enslaved Africans from sub-Saharan Africa.[1] Since the 17th century, several major outbreaks of the disease have occurred in the Americas, Africa, and Europe.[1] In the 18th and 19th centuries, yellow fever was considered one of the most dangerous infectious diseases; numerous epidemics swept through major cities of the US and in other parts of the world.[1]
In 1927, yellow fever virus was the first human virus to be isolated.[7][11]
Contents
1 Signs and symptoms
2 Cause
2.1 Transmission
3 Pathogenesis
4 Diagnosis
5 Prevention
5.1 Vaccination
5.1.1 Compulsory vaccination
5.2 Vector control
6 Treatment
7 Epidemiology
7.1 Africa
7.2 South America
7.3 Asia
8 History
8.1 Early history
8.2 Causes and transmission
8.3 Current status
9 Research
10 Notes
11 References
12 Further reading
13 External links
Signs and symptoms
Yellow fever begins after an incubation period of three to six days.[12] Most cases cause only a mild infection with fever, headache, chills, back pain, fatigue, loss of appetite, muscle pain, nausea, and vomiting.[13] In these cases, the infection lasts only three to six days.[14]
But in 15% of cases, people enter a second, toxic phase of the disease characterized by recurring fever, this time accompanied by jaundice due to liver damage, as well as abdominal pain.[15] Bleeding in the mouth, nose, the eyes, and the gastrointestinal tract cause vomit containing blood, hence the Spanish name for yellow fever, vómito negro ("black vomit").[16] There may also be kidney failure, hiccups, and delirium.[17][18]
Among those who develop jaundice, the fatality rate is 20 to 50%, while the overall fatality rate is about 3 to 7.5%.[19] Severe cases may have a mortality greater than 50%.[20]
Surviving the infection provides lifelong immunity,[21] and normally results in no permanent organ damage.[22]
Cause Yellow fever virus Ijms-20-04657-g002.webp Flavivirus structure and genome Virus classificatione (unranked): Virus Realm: Riboviria Kingdom: Orthornavirae Phylum: Kitrinoviricota Class: Flasuviricetes Order: Amarillovirales Family: Flaviviridae Genus: Flavivirus Species: Yellow fever virus Yellow fever is caused by yellow fever virus, an enveloped RNA virus 40–50 nm in width, the type species and namesake of the family Flaviviridae.[7] It was the first illness shown to be transmissible by filtered human serum and transmitted by mosquitoes, by American doctor Walter Reed around 1900.[23] The positive-sense, single-stranded RNA is around 10.862 nucleotides long and has a single open reading frame encoding a polyprotein. Host proteases cut this polyprotein into three structural (C, prM, E) and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5); the enumeration corresponds to the arrangement of the protein coding genes in the genome.[24] Minimal yellow fever virus (YFV) 3'UTR region is required for stalling of the host 5'-3' exonuclease XRN1. The UTR contains PKS3 pseudoknot structure, which serves as a molecular signal to stall the exonuclease and is the only viral requirement for subgenomic flavivirus RNA (sfRNA) production. The sfRNAs are a result of incomplete degradation of the viral genome by the exonuclease and are important for viral pathogenicity.[25] Yellow fever belongs to the group of hemorrhagic fevers.[citation needed]
The viruses infect, amongst others, monocytes, macrophages, Schwann cells, and dendritic cells. They attach to the cell surfaces 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. The capsid enters 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, causing a rearrangement of the 90 homodimers to 60 homotrimers.[24][26]
After entering the host cell, the viral genome is replicated in the rough endoplasmic reticulum (ER) and in the so-called vesicle packets. At first, an immature form of the virus particle is produced inside the ER, whose M-protein is not yet cleaved to its mature form, so is denoted as precursor M (prM) and forms a complex with protein E. The immature particles are processed in the Golgi apparatus by the host protein furin, which cleaves prM to M. This releases E from the complex, which can now take its place in the mature, infectious virion.[24]
Transmission
Aedes aegypti feeding
Adults of the yellow fever mosquito A. aegypti: The male is on the left, females are on the right. Only the female mosquito bites humans to transmit the disease. Yellow fever virus is mainly transmitted through the bite of the yellow fever mosquito Aedes aegypti, but other mostly Aedes mosquitoes such as the tiger mosquito (Aedes albopictus) can also serve as a vector for this virus. Like other arboviruses, which are transmitted by mosquitoes, yellow fever virus is taken up by a female mosquito when it ingests the blood of an infected human or another primate. Viruses reach the stomach of the mosquito, and if the virus concentration is high enough, the virions can infect epithelial cells and replicate there. From there, they reach the haemocoel (the blood system of mosquitoes) and from there the salivary glands. When the mosquito next sucks blood, it injects its saliva into the wound, and the virus reaches the bloodstream of the bitten person. Transovarial and transstadial transmission of yellow fever virus within A. aegypti, that is, the transmission from a female mosquito to her eggs and then larvae, are indicated. This infection of vectors without a previous blood meal seems to play a role in single, sudden breakouts of the disease.[27]
