Dengue Fever: Symptoms, Causes, and Prevention

What are the symptoms of dengue fever?

Dengue fever is a disease caused by a family of viruses that are transmitted by mosquitoes. Symptoms include as severe joint and muscle pain, swollen lymph nodes, headache, fever, exhaustion, and rash. The presence of fever, rash, and headache (the "dengue triad") is characteristic of dengue fever.

Typically, people infected with dengue virus are asymptomatic (80%) or have only mild symptoms such as an uncomplicated fever. Others have more severe illness (5%), and in a small proportion it is life-threatening. The incubation period (time between exposure and onset of symptoms) ranges from 3 to 14 days, but most often it is 4 to 7 days. Therefore, travelers returning from endemic areas are unlikely to have dengue if fever or other symptoms start more than 14 days after arriving home. Children often experience symptoms similar to those of the common cold and gastroenteritis (vomiting and diarrhea) and have a greater risk of severe complications, though initial symptoms are generally mild but include high fever.

Viral Replication of Dengue-

Once inside the skin, dengue virus binds to Langerhans cells (a population of dendritic cells in the skin that identifies pathogens). 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. DC-SIGN, a non-specific receptor for foreign material on dendritic cells, seems to be the main point of entry.

The dendritic cell moves to the nearest lymph node. Meanwhile, the virus genome is translated in membrane-bound vesicles on the cell's endoplasmic reticulum, where the cell's protein synthesis apparatus produces new viral proteins that replicate the viral RNA and begin to form viral particles. 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 are released by exocytosis. They are then able to enter other white blood cells, such as monocytes and macrophages.

Dengue Severe Disease-

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. It may be caused by poor binding of non-neutralizing antibodies and delivery into the wrong compartment of white blood cells that have ingested the virus for destruction. There is a suspicion that ADE is not the only mechanism underlying severe dengue-related complications, and various lines of research have implied a role for T cells and soluble factors such as cytokines and the complement system.

Dengue Warning & signs-

1) Worsening abdominal pain

2) Ongoing vomiting

3) Liver enlargement

4) Mucosal bleeding

5) High hematocrit with low platelets

6) Lethargy or restlessness

7) Serosal effusions

Dengue Prevention and Control

1) Advocacy, social mobilization and legislation to ensure that public health bodies and communities     are strengthened;

2) Collaboration between the health and other sectors (public and private);

3) An integrated approach to disease control to maximize use of resources;

4) Evidence-based decision making to ensure any interventions are targeted appropriately; and

5) Capacity-building to ensure an adequate response to the local situation.

Treatment

Apart from attempts to control the spread of the Aedes mosquito there are ongoing efforts to develop antiviral drugs that would be used to treat attacks of dengue fever and prevent severe complications. Discovery of the structure of the viral proteins may aid the development of effective drugs. There are several plausible targets. The first approach is inhibition of the viral RNA-dependent RNA polymerase (coded by NS5), which copies the viral genetic material, with nucleoside analogs. Secondly, it may be possible to develop specific inhibitors of the viral protease (coded by NS3), which splices viral proteins. Finally, it may be possible to develop entry inhibitors, which stop the virus entering cells.

Source: wikipedia