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 (Folks).
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 311).
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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