Aids Virus

THE AIDS VIRUS AIDS -- the initials stand for Acquired Immune Deficiency Syndrome -- was first diagnosed by the Center for Disease Control in Atlanta, Georgia, in 1981. It is a virus that immobilizes the victim's immune defense mechanisms, allowing such opportunistic infections as Kaposi's Sarcoma and Pneumocystis Carcinii to invade and destroy the patient. By the end of 1985, there were 14,000 reported cases and no known cure or vaccine . The virus is transmitted through semen and/or blood products with the high risk groups including sexually active gay and bisexual men, intravenous drug abusers, and their sexual partners (male or female). A highly significant climate of fear has arisen around this epidemic - significant for the lives of those infected by the virus as well as for the lives of our national and world communities as we struggle to face the ramifications of this disease. The fear is exemplified by Congressmen asking for the quarantining (read imprisonment) of AIDS sufferers; by insurance companies wanting to deny gay and bisexual men health insurance; by Evangelicals stating that this is God's punishment on an abominable life style (referring mostly to homosexuals, but also to drug abusers). What is this virus that is causing such wide-spread discomfort to the body and to the psyche? Before answering that question, let us look at how the body ordinarily protects itself from disease. The body's defense mechanism involves a complex and impressive system of recognition, communication, and action. Recognition begins in utero with an inventory of the tissues of the developing human. This inventory produces a knowledge of physiological self that will allow the baby's defense mechanisms to recognize Non-Self in the shapes of viruses, bacteria, fungi, etc. These disease-causing agents -- known as pathogens -- can be recognized by their specific protein codes known as antigens. The actions that the body can take to prevent the entrance of pathogens or to destroy them once their presence has been recognized and communicated are many. To begin with, as human beings we have species resistance (natural immunity) to some pathogens that can infect other mammals, plants or animals. Also, we have mechanical barriers, such as the skin and the mucus membranes that function to prevent infection so long as their surfaces of defense are unbroken. Enzymes, such as gastric juice in the stomach, can have a destructive effect on pathogens. A tissue response like inflammation works to prevent the spread of infection: the swelling, the heat, the redness, all indicate the increase of red and white blood cells in the area working to contain and destroy the non-self agents. Finally, we have a very specific defense mechanism known as resistance or immunity that learns to recognize the presence of specific foreign substances and thereafter continually acts to destroy them. The agents of the immune defense mechanism that operate in response to viral attack are natural killer cells, lymphocytes, and macrophages. All have their origin in the bone marrow and differentiate from a multi-potential stem cell. The macrophages evolve by means of myeloid-stem cells to macrohage precursors to macrophages, taking up posts in the skin, spleen, blood, and lymphatic tissues and fluid. The lymphocytes divide into B-lineage precursors and T-lineage precursors. The B-lymphocytes (B for "bone") will mature and travel through the blood to sites in the lymph nodes, organs, tissue, and fluids waiting for the cue to proliferate and divide into plasma cells for immediate immune response and into memory cells for long term immunity. The T-lymphocytes travel through the blood to the thymus for further education and differentiation. Released into the blood and lymph system they have two classes, T-4 and T-8, based on their recognition codes, and each class has two kinds of functions. There are: T-4 helper cells that enable many of the immune response actions to occur; T-4 inducer cells that activate the differentiation of more T-4 and T-8 cells from the T cell precursors; T-8 cytotoxic cells that do the actual destroying of virally infected cells; and T-8 suppressor cells that kick in several weeks into the infectious process to help shut down the immune response when it is no longer needed. The natural killer cells function as the first line of defense, killing virally infected cells spontaneously without interacting with the lymphocytes or having to recognize the antigen of the foreign substance. Their activity peaks in one to two days. The macrophages engulf the virus, break down its protein code and display its antigen on their cell membranes - with their own recognition device, a protein molecule encoded by a segment of the DNA known as major Histiocompatibility Complex (MHC). The B-lymphocytes function to recognize antigen circulating in the blood or lymph or displayed on the surface of an infected cell, and then to produce antibodies, proteins that bind to the antigens and aid in their destruction and removal. They divide after recognizing the antigens and produce a clone of B-lymphocytes with plasma cells secreting the specific antibody for this antigen and with memory cells encoded with the antibody formula should the virus try attacking the body again. To demonstrate how these agents interact, how the immune response of recognition/communication/action happens, let us follow a virus as it attacks the body. A virus is unique among infectious agents in that it is wholly dependent on other cells (bacterial, plant or animal) for reproduction: it must take over the DNA of a host cell and transform that cell into a factory for its own viral DNA message. So, assuming the virus has invaded the body and taken over a host cell, that virally infected cell will secrete a protein, interferon, that will stimulate the activity of the natural killer cells and of the macrophages. The macrophages will engulf and digest the virus and display the viral antigen and its own MHC (Class II) on the macrophage cell membrane. Only by recognizing both of these codes simultaneously can a T-4 cell activate more events in the immune response. This recognition by the T-4 cells plus the secretion of the protein interleukin-1 by the macrophage stimulates the T-4 cells activity. It will now secrete its own protein communication, interleukin-2, which will induce T-8 cells that have also recognized the viral antigen and the macrophage code, MHC (Class I), to proliferate. Some of the new T-8 cells will be cytotoxic and will destroy virally infected cells displaying the antigen. Other T-8 cells will be suppressor cells that act later to shut down the immune response. A T-4 helper cell that has been stimulated by the dual recognition and the interleukin-2 can also bind with a B-lymphocyte that has recognized the antigen. The B cell will mature and proliferate into clones of plasma cells producing immediate antibody and into clones of memory cells capable of producing antibody years later. B cells require the contact of the T-4 helper or the stimulation of the T-4 helper lymphokines (protein signals) to mature, grow, and differentiate. The interleukin-2 of the T-4 helper cells also bolsters the natural killer cells and the T-4's gamma-interferon stimulates the virus-engulfing and antigen-presenting activities of the macrophages. The actions of the natural killers, the macrophages, the T-8 cytotoxic cells, and the antibody of the B-plasma cells all contribute to the destruction of the virus. The T-8 suppressor cells bring the immune response to a close, and B-memory ells help prevent a reoccurrence of the viral infection later. However most of the credit for a successful defense of the body by the immune system goes to the work of the T-4 helper cells. The T-4 helper cells are exactly the cells that the AIDS virus infects. The AIDS virus has been identified as a human T-lymphotropic virus type III (HTLV-III). It is actually a retrovirus, meaning that the virus attaches itself to RNA first and using RNA as an entry, infects the DNA of a host cell. The host transcribes the viral genes and synthesizes those proteins, producing new viral cells that spread the infection. The overwhelming attraction of the HTLVIII retrovirus for the T-4 cells seem to be explained by the finding that the T-4 marker on the cell membrane, the protein that identifies the cell as "T-4," serves as the initial attachment point for the virus. (However it is also likely that macrophages, platelets, and B cells serve as reservoirs of the virus.) The consequences of the infection of the T-4 cells by the AIDS virus are nothing short of the total collapse of the immune defense mechanisms, leaving the body vulnerable to diseases tat would ordinarily be rare in the high risk population. With the onslaught of AIDS, the T-4 cells, which usually constitute 60-80% of the T cells circulating in the blood and lymph system, become too rare to detect. Without the T-4 cells to recognize antigen and communicate responses, all the other immune actions are short circuited. B cells are unable to proliferate and produce adequate antibody to contain the virus. T-8 cytotoxic and suppressor cells are similarly incapable of reproducing enough to meet the challenge. The natural killer cells and the macrophages receive no additional stimulation and are overwhelmed by the viral reproductions. The majority of AIDS victims have succumbed to Kaposi's Sarcoma, a cancer of the lining of the blood vessels, or to Pneumocystis Carinii, a protozean pneumonia, or to other diseases usually associated with immuno-suppression processes following organ transplants or involving chemotherapy. Where does the hope lie in all of this? Amidst the scrambling for research dollars on the part of scientists and physicians; amidst the controversy over whether to fund vaccine research or treatment research; amidst the cries for testing the world for HTLV-III, firing all AIDS victims, casting gay and bisexual men and IV drug users beyond the Pale -- amidst all the fear, there are individuals who are addressing the issue of AIDS, personally and globally. William Calderon, a hair stylist in San Francisco, was diagnosed as having Kaposi's Sarcoma in 1982. After an initial plunge into depression, he took control of his own recovery. He combined meditation, EST training, the visualization work of Carl Simonton, an anti-cancer diet, massive doses of vitamin C, B12, E, and Calcium, the love and support of friends, and his own will, his sense of self and self esteem to fight the disease. He claims to have his cancer in remission and his appearance, the lack of Kaposi's lesions on his body, backs up that claim. The lesson for many of us in William Calderon's experience is simple but challenging: when you seek total integration as an organism, as a self you can defeat the fragmentation of psyche/heart/body and the invasion of the non-self. The body teaches us the same lesson. When the tissues recognize non-self organisms the whole body gets behind the effort of the immune defense system to destroy the pathogens. Think of the resources -- spiritual, mental, financial, emotional, that could be rallied to the defeat of AIDS (to the defeat of our fears, our fragmentation/alienation as a species, our solipsism) if we all recognized AIDS sufferers as our own T-4 cells, as the part of our own self most vulnerable to the power of non-self. The universe is testing us... again... still. BIBLIOGRAPHY Andrews, Valerie. "Aids: Our First Planetary Illness." The Tarrytown Letter (Dec. 1985/Jan 1986), pp. 10-13. Baker Janet. Everything You Must Know About AIDS. Saratoga, CA: R&E Publishers, 1983. Fettner, Ann Guidin, and Check, William A. The Truth About AIDS, Evolution of an Epidemic. NYC: Holt, Rinehart & Winston, 1984. Gallin,, John I., MD., and Fanci, Anthony S. MD. (Eds). Aquired Immune Deficiency Syndrome (AIDS). New York: Raven Press, 1985. Helquist, Michael. "Alternative Therapies... Do They Offer Any Real Hope to People with AIDS?" The Advocate: The National Gay Newsmagazine, Vol. 435 (Dec. 10, 1985) pp. 43-47, p. 127. Hole, John W. Jr., Human Anatomy and Physiology. Dubuque: Wm. C. Brown Publishers, 1984. Lawerence, Jeffrey. "The Immune System in AIDS," Scientific American, Vol. 253 (Dec. 1985), pp. 84-93. Marrack, Phillipa and Kappler, John. "The T Cell and Its Receptor." Scientific American, Vol. 254 (Feb. 1986), pp. 36-45. Tonegawa, Susumu. "The Molecules of the Immune System," Scientific American, Vol. 253 (Oct. 1985), pp. 122-131.