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Most people recover within a week or so. In about 5% of cases, symptoms worsen and can become life-threatening. This is called severe dengue (formerly called dengue hemorrhagic fever or dengue shock syndrome). [21] [23] Severe dengue can lead to shock, internal bleeding, organ failure and even death. [24]
Dengue virus (DENV) is the cause of dengue fever.It is a mosquito-borne, single positive-stranded RNA virus of the family Flaviviridae; genus Flavivirus. [1] [2] Four serotypes of the virus have been found, and a reported fifth has yet to be confirmed, [3] [4] [5] all of which can cause the full spectrum of disease. [1]
However around 10% of those 800,000 had not had dengue fever before and therefore are at risk of severe infection because of the vaccine. [ 2 ] In the Philippines, the Dengvaxia controversy has contributed to overall vaccine hesitancy because of heightened concerns about vaccine safety.
(The world’s first dengue vaccination program, launched in the Philippines in 2016, however, was found to increase the severity of the disease for recipients of Dengvaxia who were later infected ...
By the late 1990s, dengue was the most important mosquito-borne disease affecting humans after malaria, with around 40 million cases of dengue fever and several hundred thousand cases of dengue hemorrhagic fever each year. Significant outbreaks of dengue fever tend to occur every five or six months.
[5] [18] Shock (dengue shock syndrome) and hemorrhage (dengue hemorrhagic fever) occur in less than 5% of all cases of dengue, [5] however those who have previously been infected with other serotypes of dengue virus ("secondary infection") are at an increased risk.
This year, the incidence of dengue fever globally has been the highest on record, especially in Latin American countries, where more than 9.7 million dengue cases have been reported. That's twice ...
It is not entirely clear why secondary infection with a different strain of dengue virus places people at risk of dengue hemorrhagic fever and dengue shock syndrome. The most widely accepted hypothesis is that of antibody-dependent enhancement (ADE). The exact mechanism behind ADE is unclear.