Dengue Fever is a disease that is found in developing countries. The United States does not suffer much from the disease because measures have been taken to control the population of Aedes mosquitos. These are the same mosquitos that are carriers for yellow fever (Halstead). This disease is of particular interest because it is prevalent in our neighboring countries such as those found in South America. Although it is a disease that is mainly found in developing countries, it can easily be a disease that can infect travelers from the United States. Current research is attempting to find ways to control vector human interactions, pathogenesis of Dengue, prevention and gathering a better understanding of the virus itself.
Dengue Fever can be classified as a hemorrhagic fever (Columbia Electronic Encyclopedia). The disease is caused by a single stranded RNA virus belonging to the Flaviviridae family (Malavige). There are four serotypes known as DEN 1-4 (Malavige). The viral genome is 11 kb in length, and a mature virion consists of three structures: the core, the membrane and the envelope (Malavige). In addition to these components the virus has seven non-structural proteins: NS1, NS2a, NS2b, NS3,NS4a, NS4b, and NS5 (Malavige). All of these have been implicated in the pathogenesis of severe serotypes of Dengue virus. The disease targets mononuclear phagocyte cell lineages such as macrophages and monocytes, which are all found in humans. The virus gains entry by using proteins that are located on its envelope (McBride and Pereraz).
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Humans are the primary vertebrae host for the dengue virus and female mosquitos of the Aedes subgenus stegomyia are its primary vectors (McBride). With the exception of neonatal mice, other vertebrae species are not susceptible to Dengue viruses (McBride). The virus enters the mosquitos during a blood meal from an infected human during viraemic phase of the infection (McBride). Upon entering the mosquito, the virus makes its way from the epithelium of the gut into the salivary glands. It is also possible for the virus to enter fully developed eggs of the mosquito (McBride). It is estimated that a period between 13 and 31 days occurs between successive cases in an epidemic (McBride). This is because the life cycle consists of an extrinsic incubation period in mosquitos, which is 8-12 days followed by an incubation period in humans which is 5-7 days, and the cycle repeats when a mosquito bites a viraemic human during a period of 1-12 days (McBride). By using reverse transcriptase PCR, dengue virus RNA was obtained from liver cells, and it is thought that the liver are the major site for viral replication in DHF (McBride). The Dengue virus can infect a range of cells in its host. The receptors on target cells is still not definitive, but there is no doubt that viral enveloped proteins are involved in the process (McBride). When the virus tries to gain entrance into the cell it has been shown that CD-14 associated cell surface molecule as well as non-FcR proteins play role and that the binding moieties on target cells vary between cell types and virus serotypes (McBride). Surface binding to GAGs is thought to be the first and less specific step of a multistep process involving ordered and sequential engagement of surface proteins similar to the processes found in herpes simplex-, adeno- and human immunodeficiency viruses (McBride). Replication occurs after the virus binds to the surface receptors and enters by endocytosis. The binding causes an irreversible conformational change in the enveloped from a dimer to a trimer fusing the envelope to the cell membrane releasing the nucleocapsid into the cytoplasm (McBride). The translation of the ssRNA+ occurs immediately in one open reading frame and the polyprotein is posttranslationally cleaved (McBride). This process is associated with the rough endoplasmic reticulum because it localizes the viral proteins in the luminal membrane or cytoplasmic context (McBride). NS proteins come together to for a replicase complex which binds specifically to the 3â€™ untranslated region of the viral genome making an intermediate negativesense RNA (McBride). Membranes of the RER envelope the nucleocapsids by budding and accumulation of virions occurs in intracytoplasmic vesicles (McBride). Then the mosquito vector should take its blood meal and the cycle starts a new.
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The infection can range from mild to severe. It is characterized by fever, headache and rash, but more severe infections can lead to shock and internal bleeding (McBride). The more severe form of the disease is DHF, which is caused by sudden loss of intravascular volume consequent to vascular leakage also known as hemorrhaging. When a cell is infected it begins to express NS1 on its surface. It has been suggested there is a correlation between the level of secreted NS1 in patients and the onset of Dengue Haemorraghic Fever (DHF). Patients with a higher level of sNS1 within 72 hours are at higher risk for DHF because it is thought that sNS1 contributes to circulating immune complexes associated with severe Dengue infections (Malavige). The initial infection begins with an abrupt onset of fever and myalgias. After four or five days the condition worsens by a fall in temperature where the skin becomes cold and the patients feels lethargic and restless. It is possible to die in as little as four to six hours if the pulse pressure drops and the patient becomes hypotensive (McBride). If treated around this time the patient will exhibit a maculopapular rash and sudden increase of vascular permeability (McBride). This is what causes the hemorrhaging. Complications of the disease have been attributed to DHF more so than Dengue fever. These complications include: Liver Failure, encephalopathy and myocarditis. DHF is known to have replication occur in hepatocytes and Kupffer cells which can lead to necrosis of the liver and jaundice. Necrosis of the liver will cause changes in electrolytes and hypoglycemia which can result in death. Although not as common as liver failure encephalopathy can occur in .05% of patients. Liver failure can be attributed to causing encephalopathy due to imbalances in electrolytes, but the biggest factor is edema. Dengue can cause vascular changes which can lead to the breakdown of the blood brain barrier can cause direct viral infection or cerebra edema. Myocarditis can also result from a dengue infection and causes left ventricular failure. Hypotension see in DHF and Dengue shock syndrome cause fluid overload making the left ventricle work harder causing the condition (Malavige). The immune plays a big role in the infection although it can actually make the infection worse. When a patient is infected with one serotype of the virus and survives, it grants them immunity towards that particular serotype. The downside is that if infected by a different serotype that same antibody can actually enhance the infection of the other serotype making it a more severe infection by a phenomena known as antibody dependent enhancement (ADE)(Malavige). The good news is that it only occurs in 2%-4% of individuals. In the individuals that are affected the ADE effect allows for more cells to be infected (Malavige). There is a disagreement as to which cytokines are produced by infected monocytes, but one group suggests Th1 response occurs in the first three days while a Th2 response occurs later during the infection. Another study showed that cellular immune response from T-cells can be rendered unresponsive because infection causes up regulation of IL-10 which can produce unresponsive T-cells. The virus also has the ability to infect CD4+ T cells, CD8+ T cells, and natural killer cells (Malavige). This makes the virus a difficult virus to defeat without support or treatment. Early detection is key and can be done with methods such as the tourniquet test. This tests for capillary fragility and can be use to make sure dengue fever does not manifest itself as DHF. Individuals who have dengue fever can usually recover with no problems, but it is those individuals that can later have DHF. Those individuals who get DHF are usually dengue fever survivors and have a higher mortality rate than Dengue fever because of all the complications associated with the disease. Many of the deaths attributed to DHF are in infants (Malavige). The highest mortality rate is seen with Dengue Shock Syndrome which is because of the severe plasma leakage and fluid loss. The corner stone Dengue fever management is fluid balance. There are no specific drugs that are effective against the virus one must rely on the immune system to take care of the problem. So most of the treatment is symptomatic however paracetamol is the only antipyretic recommended because others such as aspirin may cause intestinal bleeding (Malavige). The kind of fluids that should be used to replace lost fluids are debatable because some fluids work better than others. However, the WHOâ€™s official recommends crystalloid solutions. Platelet transfusion can also be used to control hemorrhaging although the most effective dose is debatable as well. Vaccines have been worked on but no effective one had been made. The best way to control dengue is to avoid the man-vector interaction. This can be done by chemical controls such as naturally occurring bug repellants. Endotoxin producing bacteria such as Bacillus thuringiensis has been approved to be used in house hold containing storages of water (Malavige). The endotoxin targets the larvae of the mosquitos. Something as simple as wearing clothes that do not expose too much skin to prevent bites can be effective although difficult because this disease affects hot tropic climates.
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Dengue viral infections now cause more illness and death than any other arboviral illness (McBride). Dengue has 100 million reported annually 90 percent of which are in children under the age of 15 (Malavige). It is important to pay close attention to this disease because over the last fifty years it has become a more prominent disease by increasing 30 fold in five of the six World Health Organization regions (Malavige). The Americas is one of those regions affected which has followed a similar trend to that of Asia with outbreaks occurring every three to four years (Malavige). The serotypes associated with outbreaks in the Americas were DEN-1 and DEN-2 (Malavige). The first major epidemic was in 1977 on the island of Cuba which was cause by the DEN-1 serotype (Malavige). It is important to note the secondary infections associated with Dengue fever can lead to a more severe condition, DHF. This was supported by subsequent outbreaks in Cuba and later Venezuela (Malavige). Unlike similar disease such as Yellow fever, Dengue can affect rural area and more urbanized area which can be a problem since spread in a more populated area can be heighten by close quarters. This disease affects tropical areas where there are many underdeveloped water management. With increase infections, it is important that these places are modernized or at least given methods to better control the vector population because Dengue virus is indiscriminate.
Dengue may seem like an obscure disease and one that not many have heard of, but it is a rising star in the world of infections diseases. With all the damages this virus can cause it is important that people in developing countries are educated on the disease and measures they can take to prevent it. It is also important information for people who love visiting tropical regions of the world because travelers beware one bite is all it takes. Although research has shed light on new mechanism that the virus uses it is important to further research in the event that a pandemic occurs.