Dengue Fever is a mosquito-borne viral disease common throughout the Caribbean and other tropical areas of the world. I am from the Virgin Islands and when I was 11 years old, I contracted Dengue Fever. So, naturally I have chosen to write about the virus that causes the illness. This paper will provide the structure and classification of Dengue virus, its life cycle, as well as the pathology and presentation of infection. Also discussed will be treatment and prevention of Dengue Fever along with the economic and public health impact of its re-emergence.
Dengue virus is classified in the Baltimore Classification System under Group IV, which consists of plus-sense, single-stranded RNA viruses (WHO, 2009). Dengue is a member of the family Flaviviridae and genus flavivirus. Its genome size is 11 kb and it is has an enveloped, icosahedral capsid. The Dengue virus species has four distinct serotypes distinguishable by antibody to antigen recognition. As with other Class IV viruses the viral RNA acts as mRNA.
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The following is a brief overview of the Dengue virus replication cycle inside mammalian host target cells. The virus attaches to the cell surface via host cell receptors. The target mammalian cells permissive to Dengue virus attachment and entry are believed to be monocytes, typically the Langerhans cells of the skin (Clyde, et.al., 2006). Immature dendritic cells are also permissive to the virus (Clyde, et.al., 2006). Entry into the cell is facilitated by receptor-mediated endocytosis. Recent research suggests that interaction between an alpha-mannose molecule on the viral E protein and DC-SIGN on the surface of mammalian target cells is responsible for allowing viral attachment (Clyde, et.al., 2006; Navarro-Sanchez et.al., 2003; Tassaneetrithep, et. al., 2003 The vesicle surrounding the virus becomes acidic and turns into an endosome. This change in acidity causes the viral envelope protein to change shape. The virion membrane and endosome membrane can then fuse so that the viral nucleocapsid can be released into the cytoplasm of the host cell. (Visit the following site for a vivid animation of Dengue fusion and entry: http://www.youtube.com/watch?v=3P2qUmg-CxI&feature=related). The nucleocapsid uncoats and viral RNA travels to the rough ER and begins protein translation using host cell ribosomes. Initially a polyprotein is made which is cleaved into three structural proteins and seven non-structural proteins. The three structural proteins are nucleocapsid(C), membrane associated protein (prM), and envelope (E). As stated earlier, the envelope(E) protein appears to be of significant importance in viral attachment to the host cell (Navarro-Sanchez et. al., 2003; Seema & SK Jain, 2005) thus enabling viral entry and infection. Of the non-structural proteins NS4B appears to be associated with the inhibition of the hostââ‚¬â„¢s IFN immune response (Munoz-Jordan, 2005) and will be considered later in the text in regards to viral clearing by the host immune system response. Viral RNA then synthesized in the cytoplasm to produce more viral genome. New viral RNA interacts with viral C protein and a new nucleocapsid is formed. The virus must pass through the ER where it gains its E and prM protein-embedded membrane. Still immature, the viral particle then goes through the Golgi apparatus and is secreted from there as a mature virus. It then leaves the cell via exocytosis. This explanation of the cycle was taken from the following website which gives a very good overview of the steps of Dengue virus replication inside mammalian host cells: http://www.who.int/tdrold/diseases/dengue/viral_rep.htm .
The presence of Dengue virus in the cell is detected by endosomal Toll-like receptors and also by RNA helicases in the cytoplasm (Munoz-Jordan, 2005). From this recognition a Type I IFN innate immune response is launched and IFN alpha and beta are upregulated (Munoz-Jordan, 2005). The IFN signals for the upregulation of STAT and it is evidenced here that the non-structural viral proteins may impede an effective immune response (Munoz-Jordan, 2005). Dengue is self limiting and the immune system does make antibodies against the particular infectious serotype.
Once infected, incubation period lasts from three days to two weeks. Symptoms of Dengue Virus infection range from mild to severe and are not often fatal. Severe symptoms include high fever, chills, pain behind the eyes, a characteristic rash, malaise, and joint pain. These symptoms persist for 4-5 days. Although Dengue Fever is self limiting, the most severe symptoms are associated with Dengue Hemorrhagic Fever (DHF) and Dengue Shock Syndrome (DSS). These two presentations can be fatal. It is believed that their virulence is contributed to by previous exposure to one of the serotypes. This implication makes an effective vaccination program challenging (Durbin & Whitehead, 2010; Stephenson, 2005).
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Treatment for Dengue fever is supportive. For the more severe presentations (DHS/DSS) hospitalization for fluid replacement and blood transfusions may be necessary. There are no effective vaccines presently available to combat the illness (Durbin & Whitehead, 2010) but development of a live attenuated vaccine is being planned (Durbin & Whitehead, 2010). Because the serotype antigens are distinct, immunity to one does not prevent re-infection by another strain. Prevention includes fumigation and repellant usage. Aedes aegypti is the main vector of transmission of Dengue virus. The virus infects both its mosquito vector and its human host. The virus exits its arthropod host via saliva, while the mosquito is feeding. Therefore, preventative efforts to control Dengue target the mosquito as well. The mosquitoes prefer to breed in standing water so one means of prevention is to exercise diligence in eliminating standing water sources around homes. One novel approach to prevention being considered is the breeding of genetically-engineered, sterile male Aedes aegypti mosquitoes and introducing them to the population. Although Aedes aegypti was almost eradicated in the Western Hemisphere in the 1960ââ‚¬â„¢s, Dengue Fever virus has become a noticeably emergent pathogen of recent years. There have been several outbreaks globally and in the Virgin Islands there is currently an outbreak of Serotype 2 Dengue virus on St. Thomas (http://www.healthvi.org/).
The economic impact of Dengue virus is not as severe in the Virgin Islands as it is in other areas of the world (Knox & Scott, 2009). The most dramatic effects seem to be in Asia and in parts of the world that are less developed (Knox & Scott, 2009). Researchers are trying to gather data suggesting that the Asian virus is more virulent and more closely associated with DHF and DSS. But in the Virgin Islands the tourism industry is a major source of income. Endemic Dengue outbreaks there will influence travel and tourism. There have been reports of Dengue infections in the US. Many of these reports stem from people who had recently arrived from or visited Puerto Rico or the Virgin Islands. Recent reports have determined the presence of the Aedes Aegypti mosquito in the Florida Keys. The future economic impact on the United States could gain significance should the virus no longer become limited to the lower Americas and the Caribbean.
These considerations of course raise issues in the Virgin Islands regarding the Public Health impact and policy. The current US Government administration is preparing to cut funding to the Dengue Research and Surveillance facility on the island of Puerto Rico. Because Dengue fever initially presents much like Influenza and because many people do not see a doctor when they become ill from Dengue fever, many doctors were not performing tests to confirm illness caused by Dengue virus. Since the recent outbreak on St. Thomas, more definitive testing has been done. Confirmation for Dengue in the Virgin Islands is done on Puerto Rico. There is concern that cuts in the budget may impact proper surveillance of Dengue virus in the territory.
While researching incidents of Dengue Fever in the Virgin Islands for this report, I did not know that an outbreak would soon occur there. From local accounts, it has been a very rainy hurricane season on St. Thomas this year. This may have contributed to the increase in Dengue Fever cases. Also, with news that the facility on Puerto Rico may lose some funding, perhaps efforts have been ramped up to encourage doctors to properly test and document Dengue Fever cases so that its endemic presence may be more noticeable and better realized. With the arrival of the Aedes aegypti mosquito near mainland US, perhaps more funding will be put into the develop a successful vaccination program against Dengue Fever. Growing up in the Virgin Islands, the prospect of contracting Dengue Fever was more of a painful nuisance than a life-threatening fear. However, DHF and DSS are bringing more sobering attention to the virulence and impact of the virus. This paper merely skims the surface of research done on Dengue fever within the last 10 years. Much has been described and proposed regarding the intricacies of cell tropism, vector-host interactions and susceptibilities, pesticides and other control mechanisms, immune response and reasons for the onset of DHF and DSS. Even the WHO has been called upon to revise the classification of the virus in light of the significance of DHF and DSS. Developing a better understanding of Dengue virus is painstakingly slow in progression at times due to the complications of variables such as who is more susceptible or which strains may be more virulent. The answers to these questions and the solutions to the effective control of Dengue virus worldwide lay in future research, better serological testing, and an increase in collaborative efforts.
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