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Pathogenesis and immunity
Humans acquire infection and become infected with the virus by the bite of Aedes mosquito vector. The leakage of plasma caused by increased capillary permeability is the major patho-physiological abnormality that occurs in dengue hemorrhagic fever and dengue shock syndrome. Bleeding, which is most important manifestation in patients with dengue hemorrhagic fever, is caused due to capillary fragility and thrombocytope-nia, and it manifests by various ways ranging from petechial skin hemorrhages to life-threatening gastrointestinal bleeding.
In the same patient on reinfection with another serotype of dengue virus, the virus antibody complexes are formed within a few days of second dengue infection. This results in an increase in viral entry and replication of a higher number of mononuclear cells followed by the release of cytokines, vasoac-tive mediators, and few coagulants. This phenomenon is called antibody-dependent enhancement and is responsible primar-ily for the disseminated intravascular coagulation seen in the patients with dengue hemorrhagic fever.
In addition, certain dengue strains particularly of dengue 2 are being considered to be more virulent. This is because more epidemics of dengue hemorrhagic fever have been associated with dengue 2 than with other serotypes.
Host immunity: Infection with dengue virus confers lifelongimmunity. The immunity is serotype specific. Infection by one serotype does not confer protection against other serotypes. The infection with dengue virus of different serotypes may cause a more severe disease, such as dengue hemorrhagic fever. Although dengue and yellow fever viruses are antigenically related, infection with dengue virus does not result in significant cross-immunity against yellow fever virus.
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