Ans. A: Aedes Aedes aegypti is the main vector for yellow fever across world Yellow fever/ "Yellow Jack" It is an acute viral hemorrhagic disease. The virus is a 40 to 50 nm enveloped RNA virus with positive sense of the Flaviviridae family. The yellow fever virus is transmitted by the bite of female mosquitoes (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. In the 19th century, yellow fever was deemed one of the most dangerous infectious diseases. Yellow fever presents in most cases with fever, nausea, and pain and it generally subsides 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. A safe and effective vaccine against yellow fever has existed since the middle of the 20th century and some countries require vaccinations for travelers. Since no therapy is known, vaccination programs are, along with measures to reduce the population of the transmitting mosquito, of great impoance in affected areas. Since the 1980s, the number of cases of yellow fever has been increasing, making it a reemerging disease Yellow fever is caused by the yellow fever virus, a 40 to 50 nm wide enveloped RNA virus belonging to the family Flaviviridae. The viruses infect amongst others monocytes, macrophages and dendritic cells. After entering the host cells, the viral genome is replicated in the rough endoplasmic reticulum (ER) and in the so-called vesicle packets. After transmission of the virus from a mosquito the viruses replicate in the lymph nodes and infect dendritic cells in paicular. From there they reach the liver and infect hepatocytes (probably indirectly Kupffer cells), which leads to eosinophilic degradation of these cells and to the release of cytokines. Necrotic masses (Councilman bodies) appear in the cytoplasm of hepatocytes. If yellow fever is suspected, the virus cannot be confirmed until six to ten days after the illness. A direct confirmation can be obtained by Reverse transcription polymerase chain reaction where the genome of the virus is amplified. Another direct approach is the isolation of the virus and its growth in cell culture using blood plasma; this can take one to four weeks. Serologically an enzyme linked immunosorbent assay during the acute phase of the disease using specific IgM against yellow fever or an increase in specific IgG-titer (compared to an earlier sample) can confirm yellow fever. Together with clinical symptoms, the detection of IgM or a fourfold increase in IgG-titer is considered sufficient indication for yellow fever. Since these tests can cross-react with other Flaviviruses, like Dengue virus, these indirect methods can never prove yellow fever infection. In a differential diagnosis, infections with yellow fever have to be distinguished from other feverish illnesses like malaria. Other viral hemorrhagic fever, such as Ebola virus, Lassa virus, Marburg virus or Junin virus have to be excluded as cause. For journeys into affected areas, vaccination is highly recommended since mostly non-native people are affected by severe cases of yellow fever. The protective effect is established 10 days after vaccination in 95% of the vaccinated people 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 from a diseased patient in Ghana and is produced in chicken eggs. WHO recommends routine vaccinations for people living in endemic areas between the 9th and 12th month after bih.