The officially supported theory of AIDS as an illness caused by a continually mutating retrovirus called HIV has not led to progress in controlling the epidemic in over two decades. We are still looking for a vaccine but chances are it will never be found. We are still treating those reacting positively to a non-virus-specific test with toxic medications, but the results are less than brilliant.

The existence of long-term AIDS survivors is unexplained and unexplainable, unless we look for alternative explanations of what might cause the immune weakness observed in AIDS patients. Since the virus has never been properly isolated and since the so-called HIV test does not prove infection, it follows that something else must be wrong with those unfortunate people who have a compromised immune system.

In the following article titled Vaccines, Antibodies and the HIV Riddle, Beldeu Singh introduces a hypothesis of oxidative causation of immune weakness. The new hypothesis overcomes problems associated with proving viral causation of the syndrome but it also opens a door to specific treatments that could rapidly reverse the epidemic.

VACCINES, ANTIBODIES AND THE HIV RIDDLE
by Beldeu Singh

The human immune system is a complex and amazing array of response mechanisms to foreign bodies called antigens designed to attack and destroy them and prevent infection and disease condition.

The system is remarkably effective to antigens. An antigen is any substance that elicits an immune response, including a virus and parts of broken protein molecules. Non-living substances such as toxins, chemicals and drugs can be antigens.

Acquired Immunity

The effectiveness of the immune system is based on four very important aspects of its design and operation - firstly, its role in self/non-self recognition; secondly, it ability to produce a wide range of antibodies but each antibody is a specific response to an invading antigen, so it is in fact a polyclonal system that develops monoclonal responses; thirdly, its antibodies bind to specific antigens not only at the initial site of invasion or infection but work in all the fluid part of the body and fourthly, the bodies can stay on after overcoming the infection for months or years and in the case of viral infections they offer live long immunity.

Most invasions by microorganisms do not result in disease. The few microbes that manage to cross the barriers of skin, mucus, cilia, and pH are usually eliminated by the natural or innate immune mechanisms that are triggerred immediately upon pathogen entry. If the pathogen cannot be rapidly eliminated by phagocytosis, inflammation is induced with the synthesis of cytokines and acute phase proteins. This early induced response is not antigen-specific and does not generate immune memory. Only if the inflammatory process is unsuccessful at eliminating pathogen will the adaptive immune system be activated - as in the case of catching a cold and process will require several days to produce armed effector cells.

Parts of the immune system are antigen-specific and have memory. The cells recognize and mount an even stronger attack to the same antigen the next time. The self/non-self recognition is on account of having every cell display a marker based on the major histocompatibility complex (MHC). Any cell not displaying this marker is treated as non-self and attacked. The process is so effective that undigested proteins in the bloodstream are treated as antigens.

Active artificially acquired immunity refers to any immunization with an antigen. By giving a safe form of the antigen artificially, the body will produce its own antibodies and, more importantly, develop circulating, long-lived B-memory cells with high affinity B-cell receptors on their surface. If at a later date the body is again exposed to that same antigen, the memory cells will cause immediate and rapid production of the appropriate antibodies for protection.

The immune system is a system of specialized cells and organs that protect an organism from invasion and infection from bacteria, viruses and it also destroys cancer cells and foreign bodies and even elicits an immune response to broken protein molecules or those protein molecules that may be broken during the process of ingestion by macrophages and may float in the bloodstream as macrophage debris.

The organs of the immune system, positioned throughout the body, are called lymphoid organs. The lymphoid tissue is distributed in many other locations as small pockets throughout the body, such as the bone marrow and thymus. The tonsils, adenoids, Peyer's patches, and the appendix are also lymphoid tissues.

Antigens and Antibodies

An important organ of the immune system is the spleen. In it are found B cells, T cells, macrophages, dendritic cells, natural killer cells and red blood cells. In addition to capturing foreign bodies (antigens) from the blood passing through it, migratory macrophages and dendritic cells bring antigens to the spleen via the bloodstream. An immune response can be initiated in the spleen when any macrophage or dendritic cells present the antigen to the appropriate B or T cells. The B cells become activated and respond with the production of large amounts of antibody specific to the antigen. The spleen can be visualized as an immunologic filter of the blood.

A healthy immune system, functioning at its optimal levels keeps the body in a healthy state. If the immune system weakens, its ability to defend the body also weakens, allowing pathogens, including viruses that cause common colds and flu, to grow and flourish in the body. The immune system also performs continual surveillance for abnormal or cancer cells. Any form of prolonged immune suppression compromises the healthy functioning of the immune system and allows opportunistic infections, including TB, pneumonia and cancers to occur in the body. Immunosuppression has been reported to increase the risk of certain types of cancer.

The immune system can be made to elicit an immune response artificially. Active artificially acquired immunity refers to any immunization with an antigen. By giving a safe form of the antigen artificially, the body will produce antibodies. Viral vaccines such as for smallpox can cause the immune system to develop circulating, long-lived B-memory cells. If at a later date the body is again exposed to that same antigen, the memory cells will cause immediate and rapid production of the appropriate antibodies for protection.

Most vaccine-preventable diseases are caused by viruses. Vaccines to help prevent these diseases generally contain weakened or killed viruses specific to the disease. There are a series of steps that the body goes through in fighting these diseases: First, a vaccine is given by a shot. Next, over the next few weeks the body makes antibodies and memory cells against the weakened or dead viruses in the vaccine. Then, the antibodies can fight the real disease-causing viruses in the person.The antibodies destroy the viruses and the person will not become ill. We learned that in school.

We also learned in school that an antibody is a protein produced by the immune system, in response to invading or foreign bodies introduced into the body, to identify and neutralize these foreign bodies such as bacteria and viruses. Each antibody recognizes a specific antigen unique to its target.

Antibodies are synthesized and secreted by plasma cells which are derived from the B cells of the immune system. The B cells are activated upon binding to their specific antigen and differentiate into plasma cells that will produce the immunoglobulins (which are glycoproteins in the immunoglobulin superfamily) that function as antibodies.

Antibodies are therefore produced in clonal lines that are specific to only one antigen, e.g., a virus hull protein. In binding to such antigens, they can cause agglutination and precipitation of antibody-antigen products ready for phagocytosis by macrophages and other cells or block viral receptors and stimulate other immune responses such as the complement pathway.

Antibodies that bind onto the docking sites of viruses block their docking ability to receptor sites on cell membranes. Being unable to dock to a cell, they cannot infect it. Antibodies can also agglutinate them so the phagocytes can capture them. Antibodies that recognize bacteria mark them for ingestion by macrophages. Activated macrophages are also capable of directly destroying tumor cells. Together with the plasma component complement, antibodies can kill bacteria directly. Antibodies also neutralize toxins by binding with them.

Antibodies are found in the blood and tissue fluids. In some cases they may be aided by T-helper cells to fight foreign bodies. They cannot attack pathogens within cells. Certain viruses "hide" inside cells (as part of the lysogenic cycle) for long periods of time and avoid the binding action of antibodies. The chronic nature of many minor skin diseases (such as cold sores) is due to this "hiding" mechanism. Any further outbreak is quickly suppressed by the immune system, but the infection is never truly eradicated in such cases because some cells retain viruses that may resume their replicating activity later on.

Antibodies and memory cells stay on guard in the body for years after the vaccination to safeguard it from the real disease germs. This protection is called immunity.

In the case of all bacterial vaccines, immunity doesn't last long and thus the vaccine needs frequent repetition to be effective, which means you are exposed to the risk again and again, unlike viral vaccines which provide years, probably a lifetime, of immunity.

Cancer Immunotherapy

Humans and mammals, including dogs, cats and mice have the ability to make antibodies that 'recognize' virtually any antigenic determinant (epitope) and bind to it. Additionally, antibodies are so specific that they discriminate between even similar epitopes. These two characteristics provide the basis for protection against disease organisms and make antibodies attractive candidates to target other types of molecules found in the body, such as: receptors or other proteins present on the surface of normal cells molecules or that may be present uniquely on the surface of cancer cells.

Monoclonal antibodies can be produced in a laboratory. Monoclonal antibodies are made by injecting human cancer cells, or proteins from cancer cells, into mice so that their immune systems develop antibodies against the injected foreign antigens (bodies). These new antibodies will bind to specific proteins on the surface of certain cells and T4 cells can identify them easily and attack them. Once bound, the cancer cells are marked for destruction by macrophages and the binding action activates the immune system to attack and kill the cells to which the monoclonal antibody is bound. It is an interesting approach in immunotherapy.

There are clearly identified processes in immunotherapy that destroy cancer cells. In one process, macrophages and natural killer cells engulf the bound tumor cell. Macrophages destroy cancer cells by ingestion using enzymes while natural killer cells secrete cytokines that lead to cell death. In the second process, when the "complement system" is initiated, also known as the 'complement cascade', the attack is confined to the cell membrane of the cancer cell resulting in a hole within the cell membrane, causing cell lysis and death of the cancer cell. Natural killer cells have a smart mechanism to kill infected cells. They insert the pore-forming molecule perforin into the membrane and then inject cytotoxic granzymes to kill the targeted cell.

Before they can engulf pathogens, phagocytes must first bind them. Pathogen surfaces generally have sugar molecules in repeating patterns (orientation and spacing) not found on host cells that can be recognized by cells of the innate immune system. Once the antigen is bound, the phagocyte extends pseudopodia around the antigen and engulfs it, forming a phagocytic vesicle (phagosome). Cytosolic vesicles called lysosomes containing digestive enzymes at low pH fuse with the phagosomes to become phagolysosomes, whose enzymes digest the antigen. This process is called phagocytosis. Some bacteria are resistant to hydrolytic enzymes and low pH and can escape from or even live in the phagolysosome. Pathogens are generally completely digested by neutrophils.

Natural killer (NK) cells function as effector cells that directly kill certain tumors such as melanomas, lymphomas and viral-infected cells, most notably herpes and cytomegalovirus-infected cells. Natural killer cells, unlike the CD8+ (killer) T cells, kill their targets directly without a prior "conference" in the lymphoid organs. However, NK cells that have been activated by secretions from CD4+ T cells will kill their tumor or viral-infected targets more effectively.

Natural killer cells are specialized cells that kill both cancer cells and cells that are harboring viruses. Their numbers increase with exercise, and supplementation with DHEA, thymus extract, vitamin E, selenium, beta-carotene, glutamine, and arabinogalactan. Their numbers fall with malnutrition, stress, alcoholism, inadequate sleep, and in people with chronic fatigue syndrome and other illnesses, drug abuse and in heavy smokers.

In addition to their hydrolytic enzymes, phagocytes use two oxygen-dependent killing systems (oxidative burst) to kill microorganisms by oxidizing and inactivating key enzymes. Macrophages depend primarily on the peroxidase-independent system, using hydroxyl radicals (OH-), superoxide anions (O2-), singlet oxygen (O-) and hydrogen peroxide (H2O2). Neutrophil myeloperoxidase interacts with H2O2 plus intracellular halides to form toxic oxidants such as OCl-. Activated macrophages also kill pathogens with nitric oxide (NO), defensin peptides, lysozyme, and secreted molecules that compete with the microbes for essential nutrients such as iron and the enzyme cofactor vitamin B12. Toxic products of macrophages and neutrophils can be used inside the phagolysosome to kill the pathogen or, when the pathogen cannot be engulfed, can be excreted for extracellular killing. The latter process often results in damage to surrounding host cells as well as to the pathogen.

Nitric oxide (NO) has broad-spectrum antimicrobial properties and is also synthesised by the endothelium of the major blood vessels. Endothelial health and secretions of NO in proper amounts is a science that will gain prominence in developing future therapies and will become a vital concept in health. It is an ubiqutious molecule in mammalian biochemistry and is involved in the development of disease states.

Cancer cells may spread into the central nervous system, testicles or other organs not easily reached with chemotherapy. These areas are often referred to as sanctuary sites. Since many drugs are unable to penetrate into these areas and destroy the cancer cells, immunotherapy may be applied as an alternative.

Cytotoxic T cells (CTL) mediate antigen-specific, MHC-restricted cytotoxicity and are important for killing intra-cytoplasmic parasites that are not accessible to secreted antibody or to phagocytes. Examples include all viruses, rickettsias, some obligate intracellular bacteria (Chlamydia) and some protozoan parasites. The only way to eliminate these pathogens is to kill their host cells. Activated T cells perform their effector functions when they encounter MHC-presented peptide on their target cells. Cytotoxic T cells activated by endogenous antigen, identify and kill the infected cells while helper T cells are activated by exogenous antigen to stimulate macrophage killing of endosomal pathogens.

Vaccination and Autoimmune Disease

The remarkable specificity of antibodies makes them interesting for study in medical science. The response of the immune system to any antigen, even the simplest, is polyclonal, which means, the immune system produces antibodies of a great range of structures both in their binding regions as well as in their effector regions. Hence, the interest in vaccines.

Vaccines have been useful in preventing viral diseases such as smallpox but vaccines pose challenges of their own. There is some evidence to suggest to even the most ardent vaccine supporter that there are risks to vaccination. The only thing that does immunize (i.e. enable the body to protect itself from harm by foreign organisms) is Mother Nature, provided she is properly supported with sufficient basic nutrition, and her sophisticated immune development process not interfered with (Vaccination Information Service;).

The term "immunisation", often substituted for vaccination, is false and should be legally challenged, because the direct injection of foreign proteins and other toxic material (particularly known immune-sensitising poisons such as mercury) sensitises, meaning makes the recipient more, not less, easily affected by what he/she encounters in the future. This means they do the OPPOSITE of immunise, commonly even preventing immunity from developing after natural exposure. (Vaccination Information Service;).

According to leading canine vaccine researcher Dr. Ronald Schultz, Chair of the Department of Pathobiology at the University of Wisconsin - Madison School of Veterinary Medicine, and editor of the textbook Veterinary Vaccines and Diagnostics, It is becoming increasingly more evident that it is no longer true to say, 'Well, even if the vaccine doesn't help, it won't hurt.'

A few years ago, the Colorado State University School of Veterinary Medicine became the first veterinary college to issue a vaccination schedule that recommended against annual vaccinations. Of particular note in this regard has been the association of autoimmune hemolytic anemia with vaccination in dogs and vaccine-associated sarcomas in cats ... both of which are often fatal (cf Re-Vaccination: Vaccination for Previously Vaccinated Dogs and Older Puppies By Christie Keith)".

In cats, there is an alarming incidence of injection site sarcomas, an aggressive and often fatal cancer. In dogs, there is a correlation between autoimmune hemolytic anemia and vaccination (Dodds, 1985; Duval and Giger, 1996), and an ongoing study at Purdue University has found that vaccinated dogs, but not unvaccinated controls, have formed antibodies to their own cells (Larry T. Glickman, DVM, "Weighing the Risks and Benefits of Vaccination," Advances in Veterinary Medicine, Vol. 41, 2001). Immunocompromised dogs vaccinated for canine distemper have been reported to develop post-vaccinal encephalitis (Meyer, "Vaccine Associated Adverse Events," Veterinary Clinics of North America, May 2001). Dogs with inhalant allergies are known to worsen after vaccination (Frick and Brooks, 1983; cf Re-Vaccination: Vaccination for Previously Vaccinated Dogs and Older Puppies By Christie Keith).

So, the problems that can be caused by vaccinations are autoimmune disease conditions and vaccine associated sarcomas. It is important to note the research that points to the fact that the direct injection of foreign proteins and other toxic material (particularly known immune-sensitising poisons such as mercury) makes the recipient more, not less, easily affected by what he/she encounters in the future. This means they do the OPPOSITE of immunise, commonly even preventing immunity from developing after natural exposure. Since vaccines use thimerosal, a compound containing organic mercury, subsequent vaccinations (especially a large number of mandated vaccinations within the first two years) cause problems not only from the free radical generating toxicity of the mercury ion (that accumulates in the tissues) but many may also suffer from its immune sensitizing effect. Thimerosal in vaccines may interfere with NO secretions by cells and in tissues and cause the wide range of problems in health.

But antibodies continue to interest scientists and in their possible role in preventing developmental defects in fetuses. Cytomegalovirus, or CMV, spreads through sex and body fluids like saliva. It often infects children and their caregivers and is the most common infection among U.S. newborns, striking about one per cent, or 40,000 babies each year. It infects most people at some point, typically with mild symptoms or none at all. But it can harm or kill fetuses and is especially dangerous when women acquire it during pregnancy.

Up to 20 per cent of infected fetuses die before or soon after birth, or have severe damage, including small heads, abnormal brains, mental retardation, and liver and hearing damage. Others develop learning disabilities by school age.

Italian doctors, in a study, injected highly concentrated antibodies of CMV into 31 women who became infected with the virus during pregnancy and whose fetuses were known to be infected as well. Only three per cent had babies with CMV damage, compared with half of the 14 women who refused the treatment. A second group of 37 women whose babies were suspected of being infected also received the treatment. Sixteen per cent had babies with CMV damage, versus 40 per cent of women in a comparison group who didn't get the treatment. The results were published in the New England Journal of Medicine by researchers at Virginia Commonwealth University .

Experts said it is nearly impossible to tell what helped the babies because the women got different numbers and doses of antibody treatments and by different methods and the most interesting question is how physical damage to fetuses from the infection, clearly documented in some by ultrasound, could be reversed by the antibody treatment, given that the mothers' own CMV antibodies don't protect fetuses from infection.

The answer may lie in the fact that physical damage to fetuses is caused by developmental defects and these are in turn produced by interference by excess free radicals or excess nitric oxide secreted in the mother. They are very small compared to most molecules and pass the placental barrier to cause problems in fetal development which is primarily an environment of rapidly dividing cells. Excess free radicals and excess nitric oxide due to endothelial dysfunction, on account of oxidative stress on it, may be produced in mothers who smoke or consume alcohol or in those who may have taken immuno-toxic medication during pregnancy.

Since its discovery in 1980 as a potent vascular smooth muscle relaxant and regulator of blood pressure, NO has been found in many cell types and implicated in a variety of biological roles. Indeed, NO is involved in the health and disease of all organs and systems, including in the immnune system and disease prevention. Nitric oxide is an important bioregulator of a wide variety of physiological processes and its excess or deficiency can cause developmental defects in fetuses and infants.

Many viral toxins may exert a similar effect in excess and the administration of antibodies to viruses in pregnant mothers helps to reduce, diminish or eliminate their stress on developing tissues and dividing cells as the antibodies bind with the viral toxins and neutralize them. This also explains the variable results in different mothers. The mothers' immune system maintains a form of integrity in the sense that it responds effectively to the invasion and threat to its own body and produces adequate amounts of antibodies for its own well being. The mothers' body cannot respond to the antibody requirements in the body of the fetus and assess the additional amounts that may be required to prevent the developmental defects in the fetus.

Dr Gallo 'finds' the Virus

Antibodies and viruses have that interesting connection which has a bearing on AIDS. Dr. Gallo began to put forth his claims that he had discovered a virus (called the HIV) that he claimed was causing AIDS. Despite the fact that those efforts in isolating viruses and replicating them do not meet the accepted gold standard and no scientist has proved that such a virus actually infects and replicates in cells of the immune system, there are scientists in institutes who claim that "after entering the body, the virus rapidly disseminates, proceeding to the lymph nodes and related organs where it replicates and accumulates in large quantities. Paradoxically, the filtering system in these lymphoid organs, so effective at trapping pathogens and initiating an immune response, actually helps destroy the immune system. As healthy CD4+ T cells travel to the lymph organs in response to HIV infection, they are infected by the HIV that is harbored there."

Gallo managed at the same time to file together with his employer, the National Institutes of Health, for a lucrative AIDS test patent. However, subsequent nucleic acid sequence analyses proved Gallo's virus from 1984 to be the same as the virus discovered by Luc Montagnier in 1983. Since Montagnier had sent his virus to Gallo in 1983, it appeared that Gallo had rediscovered Montagnier's virus. In addition, a legal investigation proved that the photograph of HIV in Gallo's first AIDS papers was that of Montagnier's virus "inadvertently" used "largely for illustrative purposes" (p. 210-11)(On Virus Hunting; review by Peter Duesberg).

The story started in 1975. "By 1975 his [Gallo's] lab had finally isolated a retrovirus from human leukemia cells. [HL23V] Gallo... faced humilation when he presented the finding at the Virus-Cancer program's yearly conference. Other scientists had tested his virus and discovered it to be a mixture of contaminating retroviruses from woolly monkeys, gibbon apes and baboons. Gallo tried to save his reputation, speculating wildly that perhaps one of the monkey viruses caused the human leukemia. In 1980 Gallo was finally credited for discovering a genuine human retrovirus, HTLV-I, which he blamed for a leukemia in blacks from the Caribbean. But he ran into trouble trying to find the virus in American leukemia patients. At the same time, a Japanese research team reported isolating a human retrovirus from leukemic patients, which they named ATLV. After they courteously sent Gallo a sample of the virus to compare with his own, Gallo published the genetic sequence of HTLV-I. The sequence of Gallo's Caribbean virus proved to be nearly identical to the Japanese virus; it contained a mistake identical to the one made by the Japanese group. Since all other non-Japanese HTLV-I isolates differed much more widely from the Gallo-Japanese twins, some retrovirologists suggest Gallo may have offered the Japanese sequence as his own. No formal investigation has probed this incident, and Gallo was awarded the prestigious Lasker Prize as the presumed discoverer of the leukemia virus." (Inventing the AIDS Virus, p.160).

"Gallo did not stop with his first human retrovirus. He isolated a second one in 1982, from a cell line derived from a patient ... But since that time HTLV-II has been retrieved from only one other patient with a similar leukemia, while plenty of cases have been found without the virus. (p.127) ... William Haseltine ... had copied the genetic sequence of HTLV-II, the second known human retrovirus, from a presentation at a science conference. He then published the sequence, unknowingly including a deliberate error planted by the Japanese research team who had actually done the work." (Inventing the AIDS Virus p.164). In 1984 Dr Gallo, presented the world HTLV-III, which was renamed HIV later, and which became known as 'the AIDS virus'.

A fundamental knowledge was necessary to be shown as the established science from the days of Pasteur and the first vaccine against the "work" of Dr. Gallo and the patents that he lodged to protect his test kit.

In 1982, Robert Gallo from the National Cancer Institute in the USA, put forward the hypothesis that the cause of AIDS is a retrovirus. One year later, Myron Essex and his colleagues found that AIDS patients had antibodies to the Human T-cell Leukemia virus Type-1 (HTLV-I), a virus discovered by Gallo a few years earlier. At the same time, Gallo and his colleagues reported the isolation of HTLV-I from AIDS patients and advocated a role for this retrovirus in the pathogenesis of AIDS (Emergency Medicine 1993;5:5-147: HAS GALLO PROVEN THE ROLE OF HIV IN AIDS?, Eleni Papadopulos-Eleopulos, Valendar F. Turner, John M. Papadimitriou). But there is no explanation why not all or a statistically significant number of AIDS patients get leukemia which is a natural expectation but instead get a host of opportunistic infections including pneumonia and sarcomas.

The most difficult aspect of the HIV postulate is to have first decided that their HIV virus is an aggressive pathogen which they claim to target the immune system itself, as HIV was said to infect the key CD4+ T cells that regulate the immune response, modifying or destroying their ability to function and to reconcile this 'science' with scientific data and evidence that some people "appear better able than others to resist progression of HIV infection or developing AIDS," resulting in "long-term survivors" who can be divided into three groups;-

1). Long-term nonprogressors who maintain healthy or steady levels of CD4+ T cells despite many years of infection

2). Those tested HIV-positive individuals who lose a significant proportion of CD4+ T cells but remain healthy, and

3). The people who remain uninfected despite repeated "exposure to HIV".

So, to save the HIV postulate for AIDS they also claim that, once the virus infects CD4+ T cells, the virus' genetic material is permanently integrated into the cell's chromosomes, establishing permanent latency within infected cells. After infection, the HIV incorporates its genetic material into the host cell DNA. If a cell reproduces itself, each new cell also contains the integrated HIV genes. The virus can hide its genetic material for prolonged periods until the cell is activated and makes new viruses. So, its not an aggressive pathogen.

They also claim that other cells act as HIV reservoirs, harboring intact viruses that may remain undetected by the immune system while it "targets" the cells of the immune system.

There is also no explaination on how an infected cell remains normal and remains undetected as an abnormal cell by NK cells or activated macrophages after the HIV incorporates its genetic material into the chromosomes of the cell. Such a virus, with such a capability, having a sophisticated enzyme system to incorporate its genetic material into the cells' chromosomes and activate it later on into replicating itself cannot be so small and illusive that it avoids isolation and replication by other virologists.

Virologist Dr Stefan Lanka states: "The rules demonstrating the existence of HIV (and retroviruses in general) were never adhered to by those who devised them nor were they ever validated." A research team at University of Western Australia claims that HIV has never been isolated so far, and questions the existence of the virus-entity. So, without a virus entity, how do you produce the test and offer it for public use? Is this politics or science?

There are too many riddles to Dr. Gallo's virus. The Japanese research team who had actually isolated viruses from some leukemia patients including the deliberate error planted by them proves a lot of science when taken together with the fact that most leukemia patients do not have such a virus. Large amounts of viral toxins could create oxidative stress on cells in the bones in persons who have low blood antioxidant levels or these viral toxins could bind micronutrients in these cells thereby shutting down the Krebs cycle and transforming them into cancer cells that have switched to the alcohol energy system. The antibodies produced could have destroyed the virus in the blood and other fluids but not in the infected cells.

Selenium and Nitric Oxide

A similar stress on the Krebs cycle whether through viral toxins or free radicals or a combination of both, suppresses it and consequently cellular function and energy output are lowered causing the chronic fatigue syndrome. Such a stress is more acute or chronic in malnourished populations and would naturally be observed more frequently in people with a low intake of selenium. Selenium is essential for the production of selenium based enzymes in the body. These enzymes are very important for mitochondrial metabolic activity and for the prevention of mDNA depletion.

Exogenous free radicals and free radical generating chemicals and pollutants, including from chemicals in cigarette smoke and very fine pollutants in exhaust fumes can cause either an excess in the production of endogenous NO or suppress its production. The body's natural balance in the production of NO is perturbed. Too little production diminishes NO required to scavenge ROS while excess NO is known to cause cell and DNA damage and induction of cGMP. In the cell, NO is capable of inducing iron depletion from iron stores, which in turn is correlated with the activation of guanylate cyclase and inhibition of mitochondrial respiration. NO has a great affnity for iron and binds readily with iron-containing proteins such as hemoglobin, myoglobin, cytochrome c, and guanylyl cyclase. NO interacts with oxyhemoglobin to form methemoglobin and nitrate.

In excess, NO can inactivate mitochondrial electron transport and ATPase. The role of oxygen reactive species in the depletion of NO and the role of NO in iron biochemistry which in turn is critical in blood cell formation in bones may provide the critical clue and link in the formation of the leukemia cell under oxidative stress coupled with imbalances in NO secretions in the body.

Chronic depletion of vitamin C in immune system cells also weakens the immune system, particularly the macrophages and the NK cells that secrete nitric oxide to destroy pathogens and cancer cells. Excess nitric oxide acts as a free radical and destroys the biochemical processes in bacteria and cancer cells but the large stores of vitamin C in these cells protect them from their own excess secretions that are in letal doses to cancer cells or invading bacteria. Hence, ingestion of large amounts of bioavailable vitamins and minerals from fruit juices and selenium intake would amount to a logical measure to boost the natural antioxidant defense biochemistry as well as to boost the health and optimal functioning of the immune system and in the prevention of opportunistic infections. This is consistent with the finding that the NK cell numbers fall with malnutrition, stress, exercise, alcoholism, inadequate sleep, and in people with chronic fatigue syndrome and other illnesses (Immune Response;). Immunotoxic medication in persons with large amounts of viral toxins and/or free radicals is a logical recipe to prevent recovery or hasten death or diminish the quality of life.

If there is no virus that has been isolated and purified according to accepted standards, what does the HIV test do? The proteins that are used in the 'HIV' test are merely the biological outcome of stressed white blood cells used in the lab and in 'Bio/Technology', June 1993, 'Aids' analyst, Dr Eleni Eleopulos exposed the non-specificity and unreliability of the 'HIV' 'antibody test'.

The disclaimer on the packaging says it is not absolute proof that a person tested positive has the virus that causes AIDS.

AIDS is acquired deficiency syndrome that can be acquired through prolonged malnutrion or prolonged use of immunosuppressants. It appears to fit more neatly into the free radical theory of AIDS or the oxidative stress theory of AIDS, incuding its progression in the individual and its "spread" in populations. Since there is a serious doubt about a specific virus that targets the cells of the immune system, when a person tests positive, it may be positive for an antibody to a broken protein that is found floating as macrophage debris, not yet filtered off in the spleen. Such protein particles may be more commonly found in people recovering from another viral attack such as flu or cold and in people recovering from parasitic infections such as malaria.

Other conditions common in underprivileged and impoverished communities that are known to cause false positive results are tuberculosis, malaria, hepatitis, and leprosy. False-positive ELISA [antibody] test results can be caused by alloantibodies resulting from transfusions, transplantation, or pregnancy, autoimmune disorders, malignancies and alcoholic liver disease.

This can be interpreted as a positive reaction to antibodies that the body may produce in other diseases or against other bodies that the body's immune system may recognize as foreign but the final analysis may just prove that it tests positive for a range of broken proteins as a result of macrophage ingestion found floating in the blood and in some white blood cells. That explains why they cannot be isolated and purified and used to reinfect other cells in which they will replicate like all other viruses.

Then there is the need to explain the antibodies which is a protective immunological response to HIV infection. People with antibodies to HIV should have protection against HIV disease, since vaccines protect by inducing the production of antibodies. However, scientists found only antibodies in HIV-positive patients, rather than the virus itself. And having found the antibodies, the proponents of the HIV postulate want the person with these antibodies to take a toxic poison like AZT and other toxic retrovirals as medication rather than declare that he is on the road to recovery like someone who has antibodies to the common flu. This compounds the HIV riddle. Any normal and healthy person taking them will probably die in 18 months and there is no record of anyone with complete recovery after taking them.

This riddle is tightly linked with the official requirement to take AZT and retrovirals after you are tested positive with antibodies which is supposed to say that you now have an immune response and are therefore safe - and that makes it bad. Yet, there are scientists at official institutes working on government funds to develop the HIV vaccine! So, when you test positive after being administered such a vaccine and are found to test positive, off you go take retrovirals and the AZT poison. Makes sense?

BELDEU SINGH


References:

Albrecht, E. W., C. A. Stegeman, et al. (2003). "Protective role of endothelial nitric oxide synthase." J Pathol 199(1): 8-17.

Nitric oxide is a versatile molecule, with its actions ranging from haemodynamic regulation to anti-proliferative effects on vascular smooth muscle cells. Nitric oxide is produced by the nitric oxide synthases, endothelial NOS (eNOS), neural NOS (nNOS), and inducible NOS (iNOS). Constitutively expressed eNOS produces low concentrations of NO, which is necessary for a good endothelial function and integrity. Endothelial derived NO is often seen as a protective agent in a variety of diseases.


Anderson, T. J. (2003). "Nitric oxide, atherosclerosis and the clinical relevance of endothelial dysfunction." Heart Fail Rev 8(1): 71-86.

The endothelium plays a key role in vascular homeostasis through the release of a variety of autocrine and paracrine substances, the best characterized being nitric oxide. A healthy endothelium acts to prevent atherosclerosis development and its complications through a complex and favorable effect on vasomotion, platelet and leukocyte adhesion and plaque stabilization. The assessment of endothelial function in humans has generally involved the description of vasomotor responses, but more widely includes physiological, biochemical and genetic markers that characterize the interaction of the endothelium with platelets, leukocytes and the coagulation system. Stable markers of inflammation such as high sensitivity C-reactive protein are indirect and potentially useful measures of endothelial function for example. Attenuation of the effect of nitric oxide accounts for the majority of what is described as endothelial dysfunction. This occurs in response to atherosclerosis or its risk factors. Much remains to be learned about the molecular and genetic pathophysiological mechanisms of endothelial cell abnormalities. However, pharmacological intervention with a growing list of medications can favorably modify endothelial function, paralleling beneficial effects on cardiovascular morbidity and mortality. In addition, several small studies have provided tantalizing evidence that measures of endothelial health might provide prognostic information about an individual patient's risk of subsequent events. As such, the sum of this evidence makes the clinical assessment of endothelial function an attractive surrogate marker of atherosclerosis disease activity. The review will focus on the role of nitric oxide in atherosclerosis and the clinical relevance of these findings.


Ando, K. (2003). "[Oxidative stress]." Nippon Rinsho 61(7): 1130-7.

Oxidative stress, which is enhanced in diabetes mellitus, causes hypertension and plays a critical role on cardiovascular damages in diabetes and hypertension. Angiotensin II is one of important intrinsic oxidants in pathophysiology of hypertension. Reactive oxygen species affect hypertension and its complications via inactivation of nitric oxide, modification of lipid metabolism, and enhanced insulin resistance. Moreover, oxidative stress and hypertension accelerate cardiovascular damages. Thus, it is important to control oxidative stress in hypertensive patients with diabetes.


Annuk, M., M. Zilmer, et al. (2003). "Endothelium-dependent vasodilation and oxidative stress in chronic renal failure: impact on cardiovascular disease." Kidney Int Suppl(84): S50-3.

Despite significant progress in renal replacement therapy, the mortality from cardiovascular disease (CVD) in patients with chronic renal failure (CRF) is many times higher than in the general population. The traditional risk factors are frequently present in CRF patients. However, based upon conventional risk factor analysis, these factors do not fully explain the extraordinary increase in morbidity and mortality in CVD among patients with CRF. Accumulating evidence suggests that CRF is associated with impaired endothelial cell function. In recent years, the role of endothelial dysfunction (ED) and excessive oxidative stress (OS) in the development of CVD has been highlighted. ED is an early feature of vascular disease in different diseases such diabetes, hypertension, hypercholesterolemia, and coronary heart disease. The precise mechanism which induces ED is not clear. Several factors however, including OS-related accumulation of uremic toxins, hypertension and shear stress, dyslipidemia with cytotoxic lipoprotein species such as small, dense low-density lipoprotein (LDL) particles, competitive inhibition of endothelial nitric oxide (NO) by increased production by asymmetrical dimethylarginine (ADMA) are pathogenic. In addition, it is known that excessive OS causes ED. An overproduction of reactive oxygen species (ROS) may injure the endothelial cell membrane, inactivate NO, and cause oxidation of an essential cofactor of nitric oxide synthase (NOS). Recent studies have demonstrated that an impaired endothelium-dependent vasodilation and OS are closely related to each other in patients with CRF.