Dengue Fever

Dr. Bhaskar Shenoy, Dr. Archana M
Dengue Fever - Introduction
Dengue fever is a globally important arboviral infection and by far the most devastating of all the recogonised arthropod transmitted virus diseases(1,2).The word” dengue” is derived from the Swahili phrase “Ka-dinga pepo”,meaning “cramp like seizure”(3).Dengue fever was reported for the first time in India in 1956 from Vellore town of Tamilnadu.(8)

The geographical areas in which dengue transmission occurs have expanded ,and they are now circulating in Asia, Africa and Americas (4).The infection is now endemic in more than 100 countries particularly the South East region, Western Pacific region, Americas (1).



The primary vector for spread of infection is Aedes aegypti, a highly domesticated day biting mosquito, with Aedes albopictus also responsible for transmission. They are Asian in origin, but also found in Africa, Europe, US (1). It breeds in clean stagnant water in containers that collect rain water. It bites several people in short period of one blood meal (8). Mosquito vector becomes infected when they feed on human during the usual 5 day period of viraemia.The virus has an extrinsic incubation period of 10 days in salivary gland, which is most rapid at high ambient temperatures. (4)The temperature rise of 1-2 degree Celsius could increase the vulnerable population by 700 million per annum (5). Mosquito that bites after the extrinsic incubation period result in infection. (4) Peak dengue transmission occurs about 6-8 weeks after peak rainfall (8).


Dengue virus belongs to the genus flavivirus within the flaviviridae family (4).The viral positive single strand RNA genome encodes 3 structural proteins the Capsid (C),membrane (M) and envelope (E) glycoprotein’s and 7 non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B and NS5).(4) The amino acid sequences of the E proteins determine the antibody neutralizing activity, that classifies DENV into 4 serotypes-DENV -1, DENV-2, DENV-3, DENV-4. (5) Humans are the main reservoir of dengue virus. (8)


Host factors that increase risk of severe dengue disease include female sex, several HLA class 1 alleles, AB blood group, single nucleotide polymorphism in TNF gene. Host factors that reduce the risk of severe dengue during second infection include race, second or third degree malnutrition, polymorphisms in FcY receptor and vitamin D receptor genes (4). The exponential increase on emergence and re-emergence of dengue fever and DHF is due to rise in population, unplanned urbanization and air travel (5).

Pathogenesis is linked to host immune response, which is triggered by infection with the virus. Primary infection is usually benign but secondary infection with different serotypes cause severe infection. (1,5) Antigen presenting dendritic cells, the humoral immune response and the cell mediated immune response are involved in pathogenesis. Proliferation of memory T cells and production of proinflammatory cytokines (Cytokine Tsunami) leads to dysfunction of luminal surface of vascular endothelium which has a layer of glycocalyx which results in plasma leakage. (1,5) There is also abundant replication of DENV’s in liver parenchymal cells, in macrophages, in lymph nodes, liver and spleen and peripheral blood monocytes. Antibody dependent enhancement (ADE) occurs when mononuclear phagocytes are infected through their Fc receptors by immune complexes that form between DENV’s and non-neutralizing antibodies. These non-neutralizing antibodies result from previous heterotypic dengue infections or from low concentrations of dengue antibodies of maternal origin in infant sera. Hence ADE theory can cause DHF in both primary infection in infants and secondary infection at any age. (4,5)

Dengue Fever Dengue Fever 06/28/2016
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