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Essay/Term paper: Aids

Essay, term paper, research paper:  Biology

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AIDS (acquired immunodeficiency syndrome) is a disease caused by a
virus- HIV (human immunodiciency virus). The first cases in this country came to
light in the early eighties. Although the origins of AIDS remains uncertain it
is thought to have emerged decades ago in sub-Saharan Africa. There is a
closely related virus (simian immunodeficiency virus, or SIV) that is found
among monkeys in that particular area which AIDS is thought to have evolved from
(Combating AIDS 353). When the virus first emerged in the United States it was
localized to the male homosexual and IV drug user communities. This
localization very quickly disappeared .
AIDS is becoming a global epidemic. No country is safe from it. There
has been AIDS cases reported around the world, in such places as the Caribbean,
Southeast Asia, Southeast Mediterranean , and Oceania. This helps to show that
AIDS knows no geographical boundries (Folks). This disease has been likened to
the Black Plaque that decimated Europe during the middle ages. By April 1984,
scientists had identified the virus responsible for AIDS and by March 1995
developed a blood test for it (Combating AIDS 355). This quick progress in the
battle even lead Heckler, the secretary of health and human services, to say
that a cure was just a few years away. Today, no cure is available and no sure
treatment for AIDS symptoms is at hand. People are still contracting and dying
from AIDS at an alarming rate. AIDS is a fatal disease that does not kill the
patient. Its principle source of infection is the HIV virus which is a
retrovirus. This means that the protein coat contains RNA instead of DNA and
when the virus injects its genetic material into the host cell, it must first
cause the cell to transcribe, using a unique enzyme called reverse transcriptase,
it into complementary- DNA (c-DNA) before replication can occur. The virus is
spherical in shape and is made of two parts: an envelop and core. The envelop
is similar to a typical cell membrane (bilipid layer) imbedded with three
proteins. The core section is bullet-shaped surrounded by a protein. Inside is
the genetic material, RNA, covered by another protein (Combating AIDS 354). The
HIV virus attacks the human helper T-cell or CD4-lymphocyte (part of the human
immune defense system). This cell normally attacks and destroys foreign
proteins and viruses. The normal CD4 T-lymphocyte is impervious to the HIV
virus but if this cell produces a CD4 receptor molecule the HIV virus then has
an entry into the cell. It attaches to the CD4 receptors on the cell surface.
A portion of the virus then penetrates the cell membrane, fuses with it and then
the HIV virus injects its core into the cell. Proteins in the core cause the
receptor cell to manufacture the viral c-DNA. This c-DNA then becomes a part of
the cells genetic material. When this happens what is known as a provirus is
formed. This provirus can remain unexpressed for years which is why a lot of
HIV positive people do not show AIDS symptoms for years. When some activator
stimulates the provirus, then viral RNA and the HIV proteins are synthesized and
new HIV viruses are produced (Nowak 964).
When activated, the virus causes a suppression of the immune system so
that one or more "opportunistic" diseases can gain a foothold. It is one of
these diseases which eventually kills the patient. An "opportunistic " disease
is one which a normal person's immune system can successfully defend against.
When something occurs that damages the immune system, then these diseases abound
One of the symptoms of full blown AIDS is dementia. This was thought to
be caused by encephalitis (inflammation of the brain). New evidence suggests
that the AIDS virus itself destroys neurons in the brain even though it does
not infect them. In laboratory findings the level of neurons in the brains of
dead AIDS patients was forty percent less than in non AIDS brains. The brains
of dead AIDS patients showed signs of HIV but the majority did not show signs of
encephalitis. It is proposed that the protein coat on HIV may interfere with
VIP (a brain protein) which some neurons need in order to send signals (Walker
There are many areas of research in determining what causes the
activation of HIV. New evidence supports the theory that there is a cofactor
involved with the accelerated onset of AIDS. This cofactor is thought to be a
mycoplasma-a primitive bacteria. The effect seems to be indirect. The
mycoplasma seems to stimulate the cell to produce substances called cytokine.
Certain cytokines are immune system simulators that are known to activate HIV.
To test the theory, scientist conducted an experiment in which human CD4
lymphocytes were infected with a mycoplasma, or HIV alone began dying off but
eventually recovered. The cells with both died off but did not recover. This
seems to indicate that something about the mycoplasma infection promotes the
growth of HIV (Ezzell 133).
Another suspected cofactor is Herpesvirus-6. This is a virus that is
normally carried by most people. It infects CD4 cells and causes them to
produce the CD4 receptor molecule. The CD4 cell, normally a killer cell is
itself destroyed by the herpesvirus-6. In those cells not destroyed, the
herpesvirus-6 may actually work in tandem with the HIV virus to destroy the
normally viral resistant CD4 cells (Fackelmann / Herpesvirus 215).
Another theory, the autoimmune theory, is proposed by Gene Shearer of
the National Institute of Allergy and Infectious Diseases states that the HIV
virus tricks the immune system into attacking itself. In an experiment, mouse
lymphocytes were inoculated into another strain of mice inducing an antibody
response against HIV but also possibly against the infected lymphocyte itself.
This response was similar to the graft vs. host response that causes many grafts
to be rejected unless the immune system is suppressed by drugs. Two other
scientists, Kion and Hoffman, of the University of British Columbia in Vancouver,
say that the HIV infection produces two effects, one against the helper cells
(CD4) and another one against the suppresser cells ( a set of immune system
cells that stabilize the helper cells) (Combating AIDS 368).
There is a lot of controversy in the theories surrounding the processes
governing the development of AIDS after a person is infected. There is a long
and highly variable incubation period with roughly fifty percent of male
homosexuals developing the disease within ten years after infection ( Folks).
One phase of research has been devoted to the body's natural immune system. In
a research project, seven young homosexual men were identified with early stag
HIV. This is normally very hard to do because most people do not get tested
until they start showing signs of the virus or other opportunistic illnesses and
by that time the virus has multiplied many times making testing of the early
stages impossible. The blood studies showed that in the first stages of the
disease, there is an enormous burst of HIV growth in the body (numbers that are
comparable to those patients with full blown, severe, AIDS). The tests taken
over the next days revealed a significant drop in the levels of the virus
population and a substantial rise in the antibody population. At full scale
antibody production, little or no HIV virus was detected. The bodies immune
system had successfully shutdown production of the HIV virus. These
researchers are now concentrating on trying to figure out why the bodies immune
system does not continuously defend against the invading HIV virus (Gorman 62).
The standard test for the HIV virus involves taking a blood sample from
the suspected individual and testing it for HIV antibodies. The body almost
always develops antibodies to viruses. It usually takes a few weeks to a few
months for the HIV antibodies to develop after infection with the HIV virus and
sometimes longer. Some reports show that it can sometimes take years for the
antibodies to show up.
Once a patient tests positive for the HIV virus, further tests are done.
One of the newest blood tests scans for an obscure adrenal hormone that seems to
forecast full blown AIDS. DHEA (dehydroepiandrosterone-a steriod) is thought to
help protect against heart disease, cancer, and viral infections among other
things. There seems to be between low levels of DHEA and the onset of full
blown AIDS. There is also some evidence that shows DHEA inhibits HIV
replication thus, helps shield against HIV progression. As a result a drug firm
is beginning to manufacture a synthetic form of DHEA to tests its help against
AIDS (Fackelmann / Mysterious 277).
There are several ways that doctors are treating the symptoms of AIDS.
As the opportunistic diseases occur, there are treated symptomatically (ex.
pneumonia is treated with antibiotics). In general most patients are treated
with AZT, a drug that though it many side effects it is thought to be effective
in slowing down the progress of the HIV virus. There is a new drug, ddI
(dideoxgenosine), available to those patients who can not tolerate AZT or for
whom it is no longer effective. DdI may also useful in combination with AZT.
The cost for ddI is about twenty percent less than that of AZT. AZT is also
used in combination with other drugs (Combating AIDS 348). Another drug that is
still in the experimental stage is Phosphorodithioate DNA. This structure is
being hailed as a potential drug in that it is hoped to interfere with the
transcribing of the viral RNA into c-DNA which is crucial for the replication of
the HIV virus. Cell culture studies of the drug have showed no toxicity at
10uM concentrations but this drug is only in the laboratory state (Cowley 70).
Another avenue of protection against HIV infection is with finding a
vaccine that will protect against HIV invasion. In 1990, a new HIV vaccine was
tested on individuals rated low risk for HIV infection. They were given a
vaccine made using a synthetic protein that mimics the protein found in the HIV
virus protein coat. The trial was a partial disappointment. The vaccine was
proven safe but seemingly none effective. It was not only none effective but it
in six recipients it caused a phenomenon that stimulates an increases in the
infectious rate of viruses. Some recipients did develop antibodies to the
protein but most of these antibodies weakened after a year. The results were
inconclusive as to whether or not the antibodies would protect against the HIV
virus (Weiss 38). Another researcher, Jonas Salk, is in the process of testing
an AIDS vaccine based on a deactivated HIV virus stripped of its protein coat
(Science and Society 34).
Although there is a lot of ongoing research into cures for AIDS and
prevention of AIDS, t


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