AIDS (acquired immunodeficiency syndrome) is a disease caused by a virus- HIV (human immunodeficiency 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 have 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 boundaries (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 leads 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 principal 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, into complementary- DNA (c-DNA) before replication can occur. The virus is spherical in shape and is made of two parts: an envelope and core. The envelope is similar to a typical cell membrane (bilipid layer) embedded 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 cDNA. This cDNA 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 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 suppressor 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-stage 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 shut down the 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 steroid) 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 through its many side effects it is thought to be effective in slowing down the progress of the HIV virus. There is a new drug, ddI (dideoxyinosine), 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 of 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 cDNA which is crucial for the replication of the HIV virus. Cell culture studies of the drug have shown 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 an effective but it in six recipients it caused a phenomenon that stimulates an increase 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).
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