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Predisposition

Severe disease is more common in babies and young children, and in contrast to many other infections it is more common in children that are relatively well nourished.[5] Women are more at risk than men.[13] Dengue can be life-threatening in people with chronic diseases such as diabetes and asthma.[13]

Polymorphisms (normal variations) in particular genes have been linked with an increased risk of severe dengue complications. Examples include the genes coding for the proteins known as TNFα, mannan-binding lectin,[1] CTLA4, TGFβ,[12] DC-SIGN, and particular forms of human leukocyte antigen.[13] A common genetic abnormality in Africans, known as glucose-6-phosphate dehydrogenase deficiency, appears to increase the risk.[22] Polymorphisms in the genes for the vitamin D receptor and FcγR seem to offer protection against severe disease in secondary dengue infection.

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Diagnosis

The diagnosis of dengue is typically made clinically, on the basis of reported symptoms and physical examination; this applies especially in endemic areas.[1] However, early disease can be difficult to differentiate from other viral infections.[5] A probable diagnosis is based on the findings of fever plus two of the following: nausea and vomiting, rash, generalized pains, low white blood cell count, positive tourniquet test, or any warning sign (see table) in someone who lives in an endemic area.[23] Warning signs typically occur before the onset of severe dengue.[8] The tourniquet test, which is particularly useful in settings where no laboratory investigations are readily available, involves the application of a blood pressure cuff for five minutes, followed by the counting of any petechial hemorrhages; a higher number makes a diagnosis of dengue more likely.[8] It can be difficult to distinguish dengue fever and chikungunya, a similar viral infection that shares many symptoms and ...
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Research

Research efforts to prevent and treat dengue include various means of vector control,[43] vaccine development, and antiviral drugs.[27] With regards to vector control, a number of novel methods have been used to reduce mosquito numbers with some success including the placement of the guppy (Poecilia reticulata) or copepods in standing water to eat the mosquito larvae.[43] There are ongoing programs working on a dengue vaccine to cover all four serotypes.[27] One of the concerns is that a vaccine could increase the risk of severe disease through antibody-dependent enhancement.[44] The ideal vaccine is safe, effective after one or two injections, covers all serotypes, does not contribute to ADE, is easily transported and stored, and is both affordable and cost-effective.[44] As of 2009, a number of vaccines were undergoing testing.[13][33][44] It is hoped that the first products will be commercially available by 2015.[27] Apart from attempts to control the spread of the Aedes mosq...
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Viral reproduction

Once inside the skin, dengue virus binds to Langerhans cells (a population of dendritic cells in the skin that identifies pathogens).[22] The virus enters the cells through binding between viral proteins and membrane proteins on the Langerhans cell, specifically the C-type lectins called DC-SIGN, mannose receptor and CLEC5A.[12] DC-SIGN, a non-specific receptor for foreign material on dendritic cells, seems to be the main point of entry.[13] The dendritic cell moves to the nearest lymph node. Meanwhile, the virus genome is replicated in membrane-bound vesicles on the cell's endoplasmic reticulum, where the cell's protein synthesis apparatus produces new viral proteins, and the viral RNA is copied. Immature virus particles are transported to the Golgi apparatus, the part of the cell where some of the proteins receive necessary sugar chains (glycoproteins). The now mature new viruses bud on the surface of the infected cell and are released by exocytosis. They are then able to en...
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