Acquired Immune Deficiency Syndrome
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Acquired Immune Deficiency Syndrome, commonly known as AIDS, is one of the leading causes of mortality in adults below age 45 in many industrialized countries, according to an article by Gebhardt, Neuenschwander and Zwahlen published in the European Journal of Epidemiology in 1998 (pNA). It is also rampant in many African nations, and is rapidly spreading in many Asian nations. AIDS is caused by the HIV virus, which destroys lymphocytes and thus compromises the immune system of the infected individual, making them highly susceptible to many infections which the normal person with an intact immune system can fend off. The virus attaches to T-helper cells with a CD4 receptor on their surface. These cells serve to activate other cells of the immune system to mount an immune response. This paper will look at the origin of AIDS, different treatments and therapies available, and current research in the field. Reports in The Economist (86) and Newsweek (Underwood 53) in 1999 both indicated that the current belief on the origin of AIDS is that it spread from chimpanzees to people in equatorial Africa. Both articles cite studies by Dr. Beatrice Hahn of the University of Alabama at Birmingham which show that the origins of HIV-1, the virus responsible for 99 percent of the world=s 33 million cases of AIDS, and confirmed a long-held belief by scientists that the virus originally came from the African primate. While other monkey species such as the sooty mangabey, which c
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i-HIV effects, as shown by Abbott=s ritonavir. (Henderson pNA). The problem with protease inhibitors is their side effects, which include diabetes and a disfiguring fat wasting/accumulation syndrome, which also seems to occur when using ritonavir. The conference did show evidence that the right combination of drugs, such as Bristol/Myers/Squibb=s stavudine/didanosine/hydroxyurea, can have a very strong and sustained anti-HIV action without relying on a single protease inhibitor. On the other hand, some immunologists believe that HIV pathogenesis may be a complex process in which small, disseminated HIV infections in localized lymphoid tissue drive the disease. If this is so, filling the blood with potent antiretrovirals may fail over time, which provides a rationale for delaying protease inhibitor therapy.
A new protease inhibitor dubbed JE-2147 kills HIV resistant to a wide variety of AIDS drugs, including other potent protease inhibitors. It has a self-adjusting element that allows it to compensate for HIV resistance mutations. This novel feature greatly delays the emergence of JE-2147-resistant HIV variants. The drug belongs to the peptidomimetic or transition-state mimetic class of HIV protease inhibitors. It is base
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Approximate Word count = 3058
Approximate Pages = 12 (250 words per page)
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