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The Dengue Virus

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In subtropical and tropical regions, the dengue virus represents a major threat to human health. The microorganism's natural hosts include mosquitoes, lower primates, and humans. Infection of the human host results in a biphasic fever with the potential to evolve into severe hemorrhagic disease. Over the past few decades, the virus genome structure, viral proteins, and viral antigens have been well characterized. Unfortunately though, the precise mechanisms by which the dengue virus causes disease remain unknown.

Throughout history, major dengue fever epidemics have generally occurred at irregular intervals within the range of the mosquito vector. For instance, in 1922, one such epidemic may have affected between 1 and 2 million people in the southern United States. At present, dengue fever may cause more human morbidity and mortality than any other arthropod-borne viral disease (Henchal & Putnak, 1990, pp. 376-396). The dengue viruses are currently endemic in most tropical areas of the world (Lanciotti, Lewis, Gubler, & Trent, 1994, p. 65). It has been estimated that there could be as many as 100 million cases of dengue infection every year (Halstead, 1988, p. 476).

The only natural hosts for dengue virus infections are mosquitoes, lower primates (e.g., chimpanzees, rhesus monkeys, and macaques), and humans. Although lower primates may develop viremias of a magnitude sufficient to infect mosquitoes, they do not generally manifest "clinically appar

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nction of this envelope is to protect viral RNA from RNases. In addition though, the lipid may also facilitate viral penetration during host cell fusion. There are two known mechanisms by which dengue viruses attach to susceptible cells. For one, the viruses may become complexed to nonneutralizing immunoglobulin G antibodies. These complexes then attach to cell surface Fc receptors on macrophages or monocytes. Second, dengue viruses may also attach to trypsin-sensitive virus receptors on host cell surfaces. Although the composition and structure of such receptors remains unknown, they could bind to "distinct regions of the E glycoprotein" (Henchal & Putnak, 1990, pp. 376-396). There are additionally two ways by which attached viruses penetrate host cells. For one, the virion envelope may merely fuse with the host cell plasma membrane. Such a process would immediately inject the nucleocapsid into the host cytoplasm. Second, the plasma membrane could invaginate to form an endocytotic vesicle around the virus. Once inside a host cell, the positive-sense viral RNA genome is initially translated to produce an RNA polymerase. The polymerase then transcribes the positive-strand RNA to a negative-strand RNA. The negative-stra
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Some common words found in the essay are:
Henchal Putnak, Dengue Virus, Hayes Gubler, RNA RNases, Gubler Trent, Ortega Tapia-Ramirez, Yuh Yang, Medical Research, dengue virus, Journal Virology, henchal putnak, putnak 1990, henchal putnak 1990, putnak 1990 pp, 1990 pp, pp 376-396, 1990 pp 376-396, July Cytotoxic, dengue viruses, host cell, dengue fever, dengue hemorrhagic fever, hemorrhagic fever, dengue hemorrhagic, al 1004 211,
Approximate Word count = 1811
Approximate Pages = 7 (250 words per page)

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