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What people say makes us excited::
January 12, 2005
By: Beldeu Singh
Independent Media TV
Anthropologists are familiar with the Piltdown Hoax and I once believed that such a hoax in science will never happen again. I was wrong.
Piltdown was an archaeological site in England where in 1908 and 1912 human, ape and other mammal fossils were found together. In 1913 at a nearby site was found an ape's jaw with a canine tooth worn down like a human's. The forgery was created by burying a skull of modern together with a jaw of an ape and the teeth on the ape's jaw had been filed down.
The general community of British paleoanthropologists came to accept the idea that the fossil remains belonged to a single creature that had a human cranium and an ape's jaw. In 1953, Piltdown 'man' was exposed as a forgery.
How had so many scientists been duped? Stephen Jay Gould offers several reasons, among them wishful thinking and cultural bias. The latter, no doubt, played a role in the lack of critical thinking among British paleoanthropologists. But, above all, the Piltdown forgery demonstrates the fallibility of scientific knowledge. Once committed to a theory, we see what fits into the theory.
The main reason Piltdown was not spotted as a fraud much earlier was that scientists weren't allowed to see the evidence, which was kept securely locked in the British Museum. Instead of focusing their attention on examining the "facts" more closely with an eye to discovering the fraud, scientists weren't even allowed to examine the physical evidence at all! They had to deal with plaster molds and be satisfied with a quick look at the originals to justify the claim that the models were accurate.
Anthropologists at that time nurtured thoughts based on the cultural prejudice that considered relatively enlarged brain, in terms of brain/body ratio, as the critical evolutionary feature that made it possible for his cultural success. This pre-conceived idea fueled the notion that the human brain must have developed to its modern size before other changes occurred in human anatomy. So, a human cranium with an ape's jaw didn't arouse as much suspicion as it would today. Fossil discoveries since Piltdown clearly show a progression from small-brained but upright posture and bipedal locomotion as the more probable path from non-simian hominids to hominids and to the larger brained and upright homo species. Scientists had "modeled the facts" that fit into their thinking and fabricated their theory.
Another reason some scientists were duped was probably because it was not in their nature to consider someone would be so malicious as to intentionally engage in such deception. Today more people worldwide have a better understanding of the nature and limits of science and we know Piltdown is little more than a wrong turn down a series of roads which, despite such detours, science eventually arrives at the right destination because of the public nature of science and the universal application of its methods. And science does get back on track.
In 1898, Friedrich Loeffler and Paul Frosch found evidence that the cause of foot-and-mouth disease in livestock was an infectious particle smaller than any bacteria. It was the first clue to the disease and nature of viruses as genetic entities that straddle in the grey area between living and non-living states.
There are thousands of different viruses that come in a variety of shapes. Most are harmless in the sense that they do not cause disease in the human body. Many viruses also cause a number of diseases in humans including smallpox, the common cold, chickenpox, influenza, shingles, herpes, polio, rabies, Ebola, hanta fever etc. These are pathogenic viruses. When they infect cells in the human body, they produce specific diseases. A chicken-pox virus does not produce AIDS or flu or polio and similarly influenza virus does not cause small-pox or rabies. Viruses are typically unable to enter cells in the presence of anti-viral antibodies the basis for the effectiveness of Jennerian vaccines.
Outside cells, viruses are inert particles floating around and are as dead as a doornail until they get to infect a plant or animal cell or a bacterial cell.
Upon attaching itself to surface of the cell wall, a virus gets its genetic material inside the cell either by tricking the host cell to pull it inside, like it would a nutrient molecule, or by fusing its viral coat with the host cell wall or membrane and releasing its genes inside. Some viruses inject their genes into the host cell, leaving their empty viral coats sitting outside. Viruses enter a cell wall that has suffered oxidative injury more easily. It is not easy for a virus to enter a healthy cell. It is susceptible to be denatured by peroxides or through the free radical mechanism of the immune cells especially through the highly reactive hydroxyl radicals.
A virus is a microscopic particle that reproduces itself inside a cell. The virus particle is really no more than a few proteins strung around a piece of RNA or DNA but without the machinery needed to replicate. So, they take control of the cell machinery and make copies of themselves. Once inside the cell, using the cellular metabolic machinery, the virus particle is disassembled. Then, using the same machinery, separate pieces of new virus are synthesized. Finally, all the viral components are put together and out come the new virus particles. The virus either destroys the cell or in the case of retroviruses the virus particles have a more orderly exit by budding out of the cell membrane. But that’s not what happens with HIV. Unlike retroviruses, HIV was said to destroy the cells.
To prove the existence of a virus you need isolate it and purify it and then infect other cells to prove the particle can make faithful copies of itself. In other words, that it can replicate.
Some viruses, like the chicken-pox virus may remain dormant inside host cells after the first infective phase for long periods, causing no obvious change in their host cells, a stage known as the lysogenic phase. But when a dormant virus is activated, it enters the lytic phase: new virus parts form, self-assemble and burst out of the host cell, killing the cell and going on to infect other cells.
Viruses are often referred to as the smallest infectious particles but some of the infective particles in plant disease lack even a viral coat and are merely small strings of plain, or "naked," RNA called viroids.
An interesting thing about Mad Cow Disease or bovine spongiform encephalopathy is that no one has been able to find for sure the infectious agent — whether it is a virus or bacterium or fungus or parasite that causes this deadly disease of the central nervous system in cattle but a virus is suspected. Small holes develop in the animals' brains, making them eventually look like big, hole-riddled sponges. Dozens of people in England are thought to have gotten a human form of BSE by eating the meat of infected cattle. The human illness is called new variant Creutzfeldt-Jakob or nvCJD.
An unusual theory has been suggested that a new kind of infectious agent, a misshapen protein - a prion. This is a radical idea because it appears impossible that a protein particle without any genes could cause infections. Proteins contain no genes —rather they are what genes code for. In other words, proteins are the products of genes in cellular activity. Now, not all scientists accept the idea that prions exist or cause the brain ailments.
Acute gastroenteritis is a common disease of adults and children worldwide and affecting 3.5 million Americans annually deserves special mention because it is not precisely defined. A general description is 1-5 days of watery diarrhea with prominent nausea and vomiting. The condition can be caused by a bewildering number of infections, drugs, toxins, and systemic diseases. Viruses are suspected when patient history and physical examinations do not point to any other agent of injury and routine stool tests for usual bacterial pathogens are negative. The pathogenesis of acute viral gastroenteritis in humans is not completely understood. The most extensive studies have been done with rotavirus
Rotaviruses attach and enter mature enterocytes at the tips of small intestinal villi. They cause structural changes to the small bowel mucosa, including villus shortening and mononuclear inflammatory infiltrate in the lamina propria. Morphologic abnormalities can be minimal. Recent studies demonstrate that rotavirus can be released from infected epithelial cells without destroying them. Viral attachment and entry into the epithelial cell without cell death may be enough to initiate diarrhea. Recent studies also suggest that one of the nonstructural viral proteins may act as an enterotoxin, promoting active chloride secretion mediated through increases in intracellular calcium concentration. Toxin-mediated diarrhea would explain the observation that villus injury is not necessarily linked to diarrhea.
After rotavirus, the most important cause of acute infantile gastroenteritis probably is caliciviruses. Astrovirus infection is associated with 2-9% of cases of infantile gastroenteritis worldwide, making it the third most frequent cause after rotavirus and calicivirus.
The epithelial cell synthesizes and secretes numerous cytokines and chemokines, which can direct the host immune response and potentially regulate cell morphology and function. Factors associated with severe and prolonged disease are immunodeficiency and immune suppression, comorbid disease, and malnutrition.
Death results from dehydration and acidosis. Acute gastroenteritis does not have a single causative factor. Pathogens include viruses and bacteria but it can also be caused by toxic medication like Vioxx or other free radical generating toxicity and two of the factors associated with severe and prolonged disease are immunodeficiency and immune suppression.
Based on the understanding of viral pathogenicity, Human Immunodeficiency Virus (HIV), after initial contact and attachment to a cell of the immune system (e.g. lymphocytes, monocytes), there is a cascade of intracellular events. The end product of these events is the production of massive numbers of new viral particles, death of the infected cells, and ultimate devastation of the immune system. But this is not the HIV theory of AIDS in a nutshell or at least the model that fits into viral pathogenicity. HIV does not kill CD4 cells - that's how Gallo got his HIV test patented (Gallo, 1985).
HIV which was said to cause AIDS presented a complex knot for proponents of the HIV-causes-AIDS to explain its infection. They presented a life cycle of HIV. HIV enters a CD4+ helper T-cell by bonding with either CXCR4 or both CXCR4 and CCR5 depending on what stage the HIV infection is in. During the early phases of an HIV infection typically both CCR5 and CXCR4 are bound while late stage infection often involve HIV mutations that only bond to CXCR4.
Once HIV has bound to the CD4+ T-cell a viral structure known as GP41 penetrates the cell membrane and the HIV RNA and various enzymes including but not limited to reverse transcriptase, integrase and protease are injected into the cell.
Since the host T-cell does not process RNA into proteins the next step is to generate DNA from the HIV RNA using the reverse transcriptase enzyme to perform reverse transcription. If this succeeds the pro-viral DNA must then be integrated into the host cell DNA using the integrase enzyme. If the pro-viral DNA becomes integrated into the host cell's DNA the cell is now fully infected but not actively producing HIV proteins. This is the latent stage of HIV an infection during which the infected cell can be an "unexploded bomb" for a potentially long time.
Once the host cell starts to produce proteins from the pro-viral DNA the HIV-supplied protease enzyme must cleave the nascent HIV proteins in order for them to be assembled into HIV virons. The virons leave the cell by budding through cholesterol rafts on the host cell surface. So, if this is it, it appears to be a replication of virons, not the virus.
In the HIV causes Acquired Immune Deficiency theory, it is accepted that HIV causes disease by infecting the CD4+ T cells. These are a subset of leukocytes (white blood cells) that normally coordinate the immune response to infection. The proponents of this theory say that by using CD4+ T cells to replicate itself, HIV spreads throughout the body and at the same time depletes the very cells that the body needs to fight the virus. Once an HIV-positive individual's CD4+ T cell count has decreased to a certain threshold, they are prone to a range of diseases that the body can normally control. These opportunistic infections are usually the cause of death.
One study showed there is no evidence that the 235 patients had a low T4 cell count due to their destruction by HIV or any other agent. In fact, at present there is no evidence that the T4 cells of haemophiliacs or for that matter, any AIDS patients, are destroyed either by HIV or any other agents, or that a causative relationship exists between a decrease in T4 cells and the appearance of the clinical syndrome. Depletion of CD4 lymphocytes has been found to be a common event that appears to be a non-specific response by the body to any type of physical or psychological stress and is often found to be below that required to diagnose AIDS in someone who is HIV-positive (Carney, 1981; des Jarlais, 1987; Feeney, 1995; Kennedy, 1988; Kiecolt-Glaser, 1984, 1991, 1992; Pariante, 1997; Williams, 1983).
There are people with AIDS with normal CD4 cell counts and healthy people with low CD4 cell counts. In a large sample, it may well be true that low CD4 cell counts identify a group of people who are more likely to be in ill health, but this logic does not apply to all individuals. There are many cases of people with AIDS defining conditions, or at least AIDS-defining low CD4 cell counts, who are continuously negative for HIV antibodies. Even if low CD4 cell counts were always associated with ill health, it is illogical to artificially raise these counts with toxic drugs but a nutrition based approach may be more beneficial.
Fawzi WW et al. reported the effect of providing vitamin supplements to human immunodeficiency virus-infected, lactating mothers on the child's morbidity and CD4+ cell counts, (Clin Infect Dis. 2003 Apr 15;36(8):1053-62). A total of 1078 human immunodeficiency virus (HIV) type 1-infected women from Tanzania were randomized in a placebo-controlled trial using a factorial design to examine the effects of supplementation with vitamin A (preformed vitamin A and beta carotene) and/or multivitamins (vitamins B, C, and E). Supplements were given during pregnancy and lactation. Children of women in the multivitamin groups had a significantly lower risk of diarrhea than did those in the no-multivitamin arm. The mean CD4+ cell count was 151 cells/microL, higher among children in the multivitamin groups than among those in the no-multivitamin group [although not with Vitamin A), indicating that CD4 cell counts can be increased in ways other than giving anti-HIV drugs.
"There are reports of drug addicts who gave up drugs and started to live a healthier lifestyle and their antibody tests reverted to negative. Their T4s returned to normal. And most telling of all, they were alive twenty years later to tell the tale," (Dr.VF Turner).
Two years before the virus that causes AIDS was discovered, physicians in the United States and Europe noticed the loss of a specific immune system cell population, called CD4 cells. It was thought to be the defining symptom of the mysterious new disease. Today, we know that one of the key defining symptoms of AIDS is mDNA depletion and chronic fatigue with muscle pains and it may also be characterized by low antioxidant level in the blood. Low host selenium levels results in a weak antioxidant defense system and inhibits CD4 T cell production. Excessive free radicals from exogenous sources deplete selenium and antioxidants in the body leading to low CD4 cell counts which opens up the body to opportunistic infectious pathogens. The increased pathogen populations in the blood in turn lead to further depression of serum selenium levels and further depress CD4 T cell count. Increasing the intake of vitamin antioxidants to scavenge free radicals and radicals reduces selenium depletion and the CD4 cell count improves.
Hence, if vitamins supplements include selenium, the results may be better not to mention the need to grow food, fruits and vegetables using selenium rich fertilizers that are also rich in other minerals.
The first odd cases of pneumocystis carinii pneumonia (PCP), a rare protozoal pneumonia, and Kaposi's sarcoma, a skin tumor that usually afflicts old men of Mediterranean descent, began showing up among young gay men in New York, San Francisco and Los Angeles in 1979. It appeared as an inexplicable anomaly. To the medically trained mind, the first thing is to look for pathogens and epidemiologist began to suspect that a mysterious new pathogen was on the loose. When the disease showed up in other populations - junkies, hemophiliacs, Haitians and blood-transfusion and organ transplant recipients - it became AIDS. And, with the gay population as a high risk group in focus, it appeared to be spread via semen via semen and blood. So they decided to look for a virus.
No one bothered to consider the obvious and common factor in these two unrelated groups with different lifestyles and behavioral risks. In old men, aged (60-70), the antioxidant levels are low - only about 20% of their peak levels during the prime of youth but they get the same amount of free radicals in the skin generated by UV band in sunlight. The gay population is exposed to free radical generating sexual lubricants and the high anal absorption rates of talc and silicone used as lubricants in condoms. Different groups have their respective exposures to free radical generating chemicals or drugs or medication, all of which deplete the antioxidants in the body and weakens the antioxidant defense mechanism and depletes antioxidant minerals to an extent that it also inhibits T4 cell formation. AIDS, therefore appears more like a deficiency in the antioxidant defense mechanism that precipitates disease or disease condition.
Ultraviolet radiation can cause genetic mutations, DNA strand breaks, and DNA cross-links. It is also known to induce DNA lesions in the dimers (cyclobutane pyrimidine) in human skin. Ultraviolet radiation causes an increase in the melanin pigmentation of skin, which may absorb much of the radiation. Melanin production also reduces with advancing age. With reduced melanin protection and a resulting increase in UV-generated free radicals and a significantly low antioxidant levels in older people, the higher the risk of skin diseases and skin cancers in them.
The proponents of the HIV-AIDS theory remained committed to that hypothesis. They focused on looking for a pathogen and they are also the proponents of the use of antiretroviral drugs. They proposed the argument that "the common notion that HIV is a killer feasting on T cells is not true. If HIV were a killer virus, it would have died out soon because there would be too little time for new infections. HIV stays in the body for years, infecting people through unsafe sex, blood transfusions and breastfeeding of infants by mothers oblivious to their infection. HIV can survive even when drugs eliminate all detectable virons in the blood (viremia). It integrates itself into the DNA of the host cell and can stay there for years, lying dormant, immune to all kinds of therapy because it is just DNA. When the cell divides and the DNA is copied, the virus is copied too. After years, the virus can become active again, seize the cell's machinery and replicate."
If drugs can eliminate all detectable virons in the blood (viremia), why is that HIV patients do not show a temporary recovery when all detectable virons are actually eliminated by antiretroviral drugs followed by a relapse after years when the virus becomes active again? There must be the classic remission.
One of the working hypotheses on cancers is that when the cell incorporates viral genetic information into the host cell’s chromosomes resulting in cell transformation and cancer. So if the virus integrates itself into the DNA of the host cell, the cell should transform and all HIV infected persons must die of cancers but this is not so, In fact, there are many seropositive individuals who recover after they stop taking the toxic antiretroviral medication.
The proponents of the HIV-integrates-into-host-cell-DNA theory say that when the cell divides and the DNA is copied, the virus is copied too. After years, the virus can become active again, seize the cell's machinery and replicate. This indicates a rather stable integration but it does not seem to decline cellular function and they do not isolate the enzymes required to integrate and de-integrate the virus from host cell DNA. And why not administer drugs that are anti-enzymatic to prevent integration of the virons or to de-integrate it from the host's DNA? How, a viron with so little genetic information can achieve precise integration into the host cell DNA and remain dormant without causing cell transformation or developmental defects and become active again to take over the cell machinery and replicate is indeed puzzling. If so, why do the cycles stop and not go on indefinitely?
Retroviruses do not kill the cells they invade but are latent passengers in humans and animals. HIV was claimed to be a retrovirus and that it killed cells added intrigue. As late as 1994, writing in " Harrison’s Principles of Internal Medicine", Gallo (and Fauci) taught medical students, "...there are no known human endogenous retroviruses". Then there was 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. So, a complex theory on HIV infection had to be created and to make it fit better into the facts the life cycle theory put forth, treating a virus like a parasitic infection.
Peter H. Duesberg (Ph.D. Professor of Molecular and Cell Biology at the University of California, Berkeley. Based on his research and experience with retroviruses, Duesberg challenged the virus-AIDS hypothesis in the pages of such journals as Cancer Research, Lancet, Proceedings of the National Academy of Sciences, Science, Nature, Journal of AIDS, AIDS Forschung, Biomedicine and Pharmacotherapeutics, New England Journal of Medicine and Research in Immunology. He has instead proposed the hypothesis that the various American/European AIDS diseases are brought on by the long-term consumption of recreational drugs and/or AZT itself, which is prescribed to prevent or treat AIDS.
Dr. Mohammed Ali Al-Bayati (President, Toxicologist, and Pathologist) quoting published research reported that in the USA, about 90% of AIDS cases are male homosexuals and heterosexuals and homosexual drug users. The remainder of the AIDS cases is hemophiliacs, people received blood transfusion, and infants who had drug user mothers. There are more than forty medical conditions described in these risk groups that are treated chronically with high doses of corticosteroids and/or other immunosuppressant agents. These conditions are caused by the heavy use of the illicit drugs, alcohol abuse, side effects of medications, allergic reactions to blood produces, and/ or infections. The treatment of a patient with prednisone at 60 mg per day for about three months can actually cause a severe depression in T cells counts which leads to infection with opportunistic agents (Tuberculosis, Pneumocyst carrinii, yeast infection, and others) and/ or the development of cancer (Kaposi’s sarcoma and lymphoma). These illnesses are called by the United States Center for Disease Control and Prevention (CDC) as AIDS-indicator diseases.
After spending five years researching and evaluating the published medical literature on the worldwide AIDS epidemic he concluded that HIV does not cause AIDS. His findings clearly point to the fact that HIV is a harmless virus, both in vivo and in vitro. His extensive review of the medical literature has not led him to a single individual with AIDS that was caused by HIV, nor a single person with AIDS who was cured by the treatment with the antiviral agents (AZT and protease inhibitors). On the contrary, the epidemiology and pathology of AIDS showed that agents and factors other than HIV are responsible for causing the AIDS epidemic. His findings clearly indicate that HIV is a harmless virus, both in vivo and in vitro. "My extensive review of the medical literature has not led me to a single individual with AIDS that was caused by HIV, nor a single person with AIDS who was cured by the treatment with the antiviral agents (AZT and protease inhibitors)".
On the contrary, the epidemiology and pathology of AIDS showed that agents and factors other than HIV are responsible for causing the AIDS epidemic, including high doses of corticosteroids and other immunosuppressive medication. Yet a medical text written by Fauci et al., “ Harrison's Principles of Internal Medicine” revealed that this book contains many prescriptions and recommendations for the treatment of medical conditions in AIDS risk groups that call for the use of high doses of corticosteroids and/or other immunosuppressant agents. On one hand their HIV-cause-AIDS hypothesis tells people that after the HIV infects cells in the immune system, it replicates in them and it leads to the ultimate devastation of the immune system while on the other the prescription is primarily large doses of immunotoxic and immunosuppresive "medicine"!
Anthony Fauci is the expert in both AIDS and autoimmune diseases. Let us examine his proposed medical treatments. The CDC and Fauci assume that HIV causes autoimmune disease but consider thrombocytopenia as AIDS-indicator illness. This assumption is wrong because AIDS and autoimmune disease are mutually exclusive illnesses. Patients with AIDS suffer from immune incompetence or reduction in the immune system functions, while patients with autoimmune disease suffer from hyper-immune system functions.
On page 731, the book states that many common drugs cause thrombocytopenia. These include chemotherapeutic agents, alcohol, myelosuppressive drugs, thiazide diuretics, estrogens, antibiotics, sedative, hypnotics, anticonvulsants, aspirin, sulfa drug, digitoxin, phenytoin, gold salts, and heparin. On page 867 the authors report that sulfnamides and trimethoprim (the treatment for pneumocyst carrinii) cause severe hematologic complications, including agranulocytosis, hemolytic and megaloblastic anemia, and thrombocytopenia. The treatment for thrombocytopenia appears on page 732 as follows: A 60 mg prednisone is administered for 4 to 6 weeks and then decreased slowly for over another a few weeks. Cyclophosphamide, azathioprine, and AZT are also among the drugs recommended for the treatment of thrombocytopenia. This treatment for thrombocytopenia can cause AIDS as shown in the following reported case. An 18-year-old woman with thrombocytopenia was treated with a steroid for 42 months. She subsequently developed Kaposi’s sarcoma that spread to the spleen.
An interesting element in AIDS is the opportunistic infections that occur after the immune incompetence or immune suppression which is now used as "AIDS defining illness". Pneumocystis carinii (PC) is one of the opportunistic infection classified by the CDC as an AIDS-defining disease but so is TB. Dr. Mohammed Ali Al-Bayati's review of the medical literature showed that this disease has existed long before HIV. Fauci et al. reported that Pneumocystis carinii is an opportunistic pathogen whose natural habitat is the lung and this organism is an important cause of pneumonia in the compromised host. Pneumocystis carinii pneumonia occurs in premature and malnourished infants; children with primary immunodeficiency diseases; and patients receiving immunosuppressive therapy (particularly glucocorticoids) for cancer, organ transplantation, and other disorders. Symptoms often began after the glucocorticoid dose has been tapered. Sepkowitz et al. conducted a twelve-year retrospective review from a tertiary-care cancer center that included 134 HIV-negative cancer patients. Corticosteroids were found to be a significant risk factor for PCP in 116 (87%) of these patients. The median maximum corticosteroid dose was 80 mg prednisone and the median length of time receiving corticosteroids was 3 months.
Naturally, reversal of CD4+ T cells depletion in the peripheral blood was reported in HIV-positive homosexual men after the termination of their treatment with glucocorticoids. And as expected of such recovery the CD4+ T cells counts rose from 313 cells/µL to 843 cells/µL, while the viral load drop from 31,300 RNA copies/mL to 11,400 RNA copies/mL within a few weeks following the cessation of the glucocorticoid treatment and without the use of the antiviral therapy. This indicates that the viral load counts is highly influenced by the glucocorticoid treatment and the presence of other infectious agents brought on by immunotoxic or immunosuppresive "medication".
The fact is, if the immune system fights infective agents and prevents disease then any disease can take root in the organs of the body if it is suppressed or rendered incompetent by immunotoxic medication. The antioxidant defense system supports the immune system, promotes optimal cellular function and protects the cells from free radical and radical damage and malnutrition could result in oxidative damage to cell walls and oxidative injury to cellular function, thereby opening up the body to infections. Naturally drugs, chemicals and medication that have free radical generating toxicity will first deplete the antioxidants in the body and reduce the body's capacity to produce antioxidant enzymes resulting in immune competence and resulting in greater susceptibility to infections, illnesses and cancers.
Enigmatically Fauci's medical text prescribes glucocorticoid as one of the agents in the treatment for PCP on page 1825. They wrote, “Adjunct glucocorticoid therapy should be started as soon as possible after the diagnosis is made, preferably no later than 36 to 72 h”. This is puzzling because glucocorticoid compounds cause severe depression in T cell counts and the functions of the immune system but are used to treat PCP and other opportunistic infections in AIDS patients. This approach can only be described as one aimed to hasten death and cannot be scientifically justified. It definitely prolongs the life of the AIDS epidemic but not the life of the patient. Remember treatment means first to do no harm.
The enigma does not end there. Other drugs such as, sulfnamides and trimethoprim are also used in the treatment of PCP, which cause severe hematological complications, including agranulocytosis, hemolytic and megaloblastic anemia and thrombocytopenia. The results of clinical trials on AZT and protease inhibitors have revealed that these agents are poisons and not cures. AZT is a very toxic poison that promotes cancer formation in the human body. "Granulocytopenia", is a deficiency of the most numerous cells of our immune system, which in turn leads to opportunistic infections. Prolonged use of AZT attacks the immune system through free radical toxicity. There appears to be a shift in medical practice away from cures and medication that boost the antioxidant defense system and the immune system to one that is oriented towards treatment by drugs that are immunotoxic or immunosuppressive or by drugs that exhibit free radical toxicity in the human body.
While on page 731, the medical text states that many common drugs cause thrombocytopenia, including chemotherapeutic agents, alcohol, myelosuppressive drugs, thiazide diuretics, estrogens, antibiotics, sedative, hypnotics, anticonvulsants, aspirin, sulfa drug, digitoxin, phenytoin, gold salts, and heparin and sulfnamides and trimethoprim on page 867 (the treatment for Pneumocyst carrinii) cause severe hematologic complications, including agranulocytosis, hemolytic and megaloblastic anemia, and thrombocytopenia, on page 732, the text describes the treatment for thrombocytopenia : A 60 mg prednisone is administered for 4 to 6 weeks and then decreased slowly for over another a few weeks. Toxic drugs such as Cyclophosphamide, azathioprine and AZT are also among the drugs recommended for the treatment of thrombocytopenia.
Conflicts in diagnosis are best evaluated by using a differential diagnosis. It seems that Anthony Fauci and the CDC have used the exact-opposite approach when dealing with the AIDS epidemic. Fauci and his colleagues are calling the heroin induced kidney lesion that was described in their book and the medical literature as an HIV disease. Gross examined biopsies from the kidneys of 14 heroin drug users and found that 11 (79%) of them show focal segmental glomerulosclerosis. They called drug-related illnesses as HIV diseases. Interestingly, the standard treatment for nephritic syndrome in Fauci’s book (page 1541) is also high doses of glucocorticoids for two months or more and in some cases this treatment is combined with cytotoxic drug and other immunosuppressive agents. This treatment can also cause non-HIV AIDS.
The literature weighs heavily in favor of a multi-factorial free radical induced AIDS in persons who abused alcohol or abused drugs such as heroin and in persons given immunotoxic or immunosuppressive medication for prolonged use as well as in people with a weak antioxidant defense system on account of malnutrition, especially selenium deficiency rather than a virus that is pathogenic in the immune system. Hence, in most cases restoring the immune system function of the body by a broad spectrum antioxidant and mineral formula should enable patients with oxidative damage and oxidative injury associated with low CD4 counts to get back to normal within 1 to 3 months and the body is concurrently able to fight infections and be cured. This approach may not be recommended by current mainstream medical practice and largely because such formulations are relatively easy to produce in contrast to patents that protect the business and profits of pharmaceutical companies. Prolonging the HIV-AIDS hypothesis protects and serves that industry's interest better. Business thrives when it is supported by unreliable HIV-AIDS "diagnosis" based on tests which will then open up the possibility of administering large doses of patented immunotoxic medication for months until the "infected" person dies. It is a cycle that supports a USD30-40 billion industry.
Oxygen free radicals and their metabolites, collectively described as reactive oxygen species (ROS), have been implicated in the pathogenesis of many diseases. Major sources of ROS in occupational and environmental exposures include exposure to asbestos, crystalline silica, coal, chromium, herbicides, bleomycin, and cigarette smoke. "ROS-induced injury may contribute to patterns of cell injury and alterations at the molecular level by initiation, propagation, and autocatalytic chain reactions. Intracellular signalling, activation and inactivation of enzymes, stimulation, secretion, and release of proinflammatory cytokines, chemokines, and nuclear factor activation and alterations are also common events," (Environ Health Perspect 105(Suppl 1):165-177, 1997).
Recent research implicates a central role for oxygen free radicals in the initiation of cellular injury that leads to the development of diseases. It is well established that oxygen free radicals and their metabolites--collectively called reactive oxygen species (ROS)--can induce direct cell injury, which may trigger a cascade of radical reactions promoting the disease process. Furthermore, excessive generation of ROS may lead to: the stimulation of the infammatory process; secretion of chemotactic factors, growth factors, proteolytic enzymes, lipoxygenases, and cycloxygenases; inactivation of antiproteolytic enzymes; and activation of oncogenes and transcription factors. Exogenous sources of oxygen free radicals include tobacco smoke, toxic gases, vapors, chemicals, dust particles, and ambient air containing toxins. Industrial operations, congested urban environments, and automobile emissions can produce oxidative stress. Diesel emissions contain diverse, potentially toxic materials in the form of gases, metals, chemicals, and particulate matter. Many of these complete and incomplete products of combustion are known to be genotoxic, cytotoxic, fbrogenic, and/or carcinogenic.
Nitric Oxide (NO) is a short-lived radical, highly reactive and lipophilic in nature, with a very short life of a few seconds. NO is generated enzymatically in the cells by NO synthases, which are homologous to cytochrome P450 reductase. Many tissues contain this constitutive enzyme. NO may function as a scavenger for O2•- and limit O2•- radical-induced damage but in the activated alveolar macrophage, an inducible enzyme independent of Ca2+ is present. Cytokines are important inducers of NO synthase. Macrophage NO is cytotoxic to microbial cells and tumor cells. NO synthase inhibition attenuates immune complex-induced vascular injury and inflammation.
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.
Major sites of endogenous generation of ROS in the biological system are within the mitochondria, microsomes, endoplasmic reticulum, phagocytic cells, endothelial cells, and nuclei. Since lipids, DNA, proteins, and enzymes are susceptible to oxidative damage by the endogenous generation of ROS, a well-balanced antioxidant defense system protects against such damage. Conversely, excess free radicals and radicals will deplete vitamins, antioxidant minerals and antioxidant enzymes causing problems that can precipitate illnesses. And an oxidative stress in the immune system leads to AIDS; in the skin may lead to skin cancers; in the anal tissue may lead to anal lymphomas; in the lung tissue may produce lung disease; in the brain may produce depression and suicidal tendencies or brain tumors, etc.
Quite naturally oxidative stress would be higher in the urban population compared to the rural communities and tribal communities in highlands and Eskimo populations. Among the urban people the oxidative stress, on the average would be relatively higher in those using recreational drugs, sexual lubricants and immunotoxic medications. The higher incidence of AIDS coincides in these “high risk” groups. Similarly, groups with poor nutrition and selenium deficiency or low antioxidant intake will experience a higher incidence of AIDS.
In the HIV theory of AIDS, there exists a virus that causes AIDS through attacking the immune system which means it is pathogenic to cells in the immune system but no scientist has been isolate such a virus and purify it!
According to the HIV theory of AIDS, the virus is sexually transmitted and that should produce an HIV-AIDS explosion in the heterosexual population within 25 years. But it did not happen. This point is well put forth by Dr. Robert Root-Bernstein. Female prostitutes often have 200-300 sexual partners per year and are therefore assumed to have much higher rates of exposure to HIV and AIDS than the vast majority of heterosexuals. Many AIDS researchers assumed that female prostitutes would be the vectors (or means of transmission) of HIV and AIDS to the heterosexual community based on the fact that a single HIV-infected intravenous drug user or bisexual man could infect one female prostitute, who in turn could infect dozens or perhaps even hundreds of non-drug using heterosexual men. These men could, in turn, infect their other sexual partners, and an explosion of HIV and AIDS could occur among people without any obvious risk for AIDS. Paradoxically, no heterosexual epidemic has occurred and no evidence of female prostitutes transmitting HIV or AIDS into the heterosexual community exists for any Western nation. Transmission almost always seems to be drug related. In fact, sexual acquisition of HIV and AIDS among female prostitutes themselves is almost unknown in the absence of concomitant intravenous drug use. Cell-free viral particles have never been found directly in semen. In 'American Journal of Epidemiology' (Vol. 146, No.4), Nancy S. Padian et al reported: "We estimate that HIV infectivity for male-to-female transmission is low, approximately 0.0009 per contact, and that infectivity for female-to-male transmission is even lower."
In New York City, for example, 40 to 50 percent of streetwalkers (a very low caste of prostitute) who have used IV drugs over the past decade are HIV seropositive. Among call girls in New York City (a higher caste of prostitute), no seropositivity was found among those who were drug free. These figures were constant between 1984 and 1989. These statistics have significant implications on the causative factor or factors of AIDS.
HIV is not behaving like a typical sexually transmitted disease. There is only one possible conclusion: as Japanese physician Y. Shiokawa has suggested, it is probable that drug use, multiple concurrent diseases, malnutrition, and other immunosuppressive factors are required to increase susceptibility. In fact, it better fits a model based on oxidative stress in cases of malnutrition and selenium deficiency and on oxidative damage and oxidative injury to cells of the immune system and cells in organs targeted by recreational drugs or immunotoxic medication.
Many haemophiliacs who did not engage in promiscuous sexual activity or drug abuse suffered AIDS. Scientists reviewed the association between the Acquired Immune Deficiency Syndrome (AIDS) and haemophilia and carefully examined the data that have been interpreted as indicating transmission of the human immunodeficiency virus (HIV) to the recipients of purportedly contaminated factor VIII preparations. They concluded that the published data do not prove the hypothesis that such transmission occurs and therefore HIV cannot account for AIDS in haemophiliacs. It could be on account of the medication prescribed to them which must be tested for free radical toxicity in the human body.
Dr. Heinz Ludwig Sänger, Emeritus Professor of Molecular Biology and Virology and a former director of the Department of Viroid Research at the Max- Planck-Institutes for Biochemy wrote, "During the past 20 years HIV-AIDS research has shown to a line of critical scientists again and again that the existence of HIV has not been proven without doubt, and that both from a etiological (causal), and a epidemiological view, it can not be responsible for the immunodeficiency AIDS. In view of the general accepted HIV/AIDS hypothesis this appeared to me so unbelievable that I decided to investigate it myself. After three years of intensive and, above all, critical studies of the relevant original literature, as an experienced virologist and molecular biologist I came to the following surprising conclusion: Up to today there is actually no single scientifically really convincing evidence for the existence of HIV. Not even once such a retrovirus has been isolated and purified by the methods of classical virology."
The rules for isolation of a retrovirus were thoroughly discussed at the Pasteur Institute, Paris, in 1973, and are the logical minimum requirements for establishing the independent existence of HIV. They are:
1. Culture of putatively infected tissue.
2. Purification of specimens by density gradient ultracentrifugation.
3. Electron micrographs of particles exhibiting the morphological characteristics and dimensions (100-120 nm) of retroviral particles at the sucrose (or percoll) density of 1.16 gm/ml and containing nothing else, not even particles of other morphologies or dimensions.
4. Proof that the particles contain reverse transcriptase.
5. Analysis of the particles' proteins and RNA and proof that these are unique.
6. Proof that 1-5 are a property only of putatively infected tissues and can not be induced in control cultures. These are identical cultures, that is, tissues obtained from matched, unhealthy subjects and cultured under identical conditions differing only in that they are not putatively infected with a retrovirus.
7. Proof that the particles are infectious, that is when PURE particles are introduced into an uninfected culture or animal, the identical particle is obtained as shown by repeating steps 1-5.
The HIV has never been isolated and purified and there is no proof of the HIV based on this standard rules and procedure! Dr. Etienne de Harven is emeritus Professor of Pathology, University of Toronto. He worked in electron microscopy (EM) primarily on the ultrastructure of retroviruses throughout his professional career of 25 years at the Sloan Kettering Institute in New York and 13 years at the University of Toronto. In 1956 he was the first to report on the EM of the Friend virus in murine (mouse) leukemia, and in 1960, to coin the word "budding" to describe steps of virus assembly on cell surfaces. He delivered a speech at the 12th World AIDS Conference in Geneva at the session "HIV-testing: Open Questions about Specificity". He questions the isolation of HIV. Such a retrovirus has not been isolated and purified by the methods of classical virology. Virologists 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."
Professor Dr. Peter Duesberg started questioning HIV in 1987. He concluded that there is no virological nor epidemiological evidence to back-up the HIV-AIDS hypothesis. Instead, the “virus” is biochemically inactive and harmless, and AIDS is not behaving as a contagious disease. Dr. Robert Root- Bernstein, who held a MacArthur Prize fellowship from 1981 to 1986, is associate professor of physiology at Michigan State University. Dr. Robert like Duesberg conducted a thorough study of the AIDS literature and could not find any evidence to back up the claim that HIV is the cause of AIDS, that AIDS is a new disease, or that it is contagious. AIDS, according to him a multi-causal condition, could also be caused by well known risk factors.
A group of medical scientists from Perth, Australia, is also questioning HIV and AIDS. The team is headed by Dr. Eleni Papadopulos-Eleopulos, professor of medical physics at Royal Perth Hospital, a teaching hospital at the University of Western Australia. The research team claims that HIV has never been isolated so far, and questions the existence of the virus-entity.
The causal relationship between HIV and any disease is not settled. "HIV is an ordinary retrovirus. There is nothing about this virus that is unique. Everything that is discovered about HIV has an analogue in other retroviruses that don't cause AIDS. HIV only contains a very small piece of genetic information. There's no way it can do all these elaborate things they say it does," according to Dr. Harvey Bialy (Molecular Biologist and former editor of Bio/Technology and Nature Biotechnology as reported in Spin June 1992). Dr. Gordon Stewart (Emeritus Professor of Public Health, University of Glasgow) agrees that "AIDS is a behavioral disease. It is multifactorial, brought on by several simultaneous strains on the immune system - drugs, pharmaceutical and recreational, sexually transmitted diseases, multiple viral infections," (Spin June 1992). Dr. Alfred Hässig, (1921-1999) was professor emeritus in immunology at the University of Bern, Director of the Swiss Red Cross Transfusion Service, and President of the Board of Trustees of the International Society of Blood Transfusion. His Swiss research group doesn't believe that HIV causes AIDS either.
So, how did the world get duped into believing that HIV causes AIDS? Very simply but on a very serious note, one of the reasons is aptly stated by Dr. Richard Strohman (Emeritus Professor of Cell Biology at the University of California at Berkeley) when he said, "In the old days it was required that a scientist address the possibilities of proving his hypothesis wrong as well as right. Now there's none of that in standard HIV-AIDS program with all its billions of dollars," (Penthouse April 1994).
Work by scientists, shoddy clinical trials and highly improper statistics concerning HIV and AIDS have been passed off as science. Unsuspectingly, non-governmental organizations, medical practitioners and the top members of scientific establishment have carelessly supported or joined the media in spreading misinformation about the nature of AIDS and HIV as the pathogenic factor in AIDS although there are hundreds of thousands of healthy people who tested HIV-positive and live as long as HIV-negative people and there are many people with non-HIV AIDS who respond to proper nutrition.
And now, the situation as described by Dr. Roger Cunningham (Immunologist, Microbiologist and Director of the Centre for Immunology at the State University of New York at Buffalo) has become rather grave because "Unfortunately, an AIDS 'establishment' seems to have formed that intends to discourage challenges to the dogma on one side and often insists on following discredited ideas on the other," (Sunday Times (London) 3 April 1994).
And the 'establishment' has created bigger problems. There is no Universal Gold Standard 'HIV' test to prove 'HIV' positivity. The 'HIV' antibody test does not detect a 'virus' but an assortment of proteins that are non-specific to the hypothetical 'HIV'. The proteins that are used in the 'HIV' test are merely the biological outcome of stressed white blood cells used in the lab. There can be no Gold Standard 'HIV' test because there is no Gold Standard 'HIV' isolate. Methods of classical virology require that all evidence of 'HIV' positivity must be confirmed by pure culturing of a patient's lymphocytes and detection of whole, sell-free viral particles; so far this has never been achieved. 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'.
'HIV' is an artefact of cell-culture invented by Dr Robert Gallo. The phenomena collectively known as 'HIV' are non-specific: reverse transcriptase is non-specific; PCR is non-specific; Viral Load is non-specific. Each property relating to 'HIV' can be shown to pertain to the cells used in co- cultivation experiments. No particle of 'HIV' has ever been obtained pure, free of contaminants; nor has a complete piece of 'HIV' RNA (or the transcribed DNA) ever been proved to exist. Moreover, Dr David Ho admits that 99.8 per cent of putative 'HIV particles' are non-infectious; the remaining 0.2 per cent of 'viral particles', being defective, are not capable of replication. As a transmittable entity, 'HIV' could not survive in nature. This indicates that what we are calling 'HIV' is a misinterpreted, non-transmissible, endogenous epiphenomenon that should never have been classed as a virus.
Dr John Papadimitriou states that the proper controls have never been done: "They have not proven that they actually have detected a unique, exogenous retrovirus. The critical data to support that idea have not been presented. You have to be absolutely certain that what you have detected is unique and exogenous, and a single molecular species...('Aids: The failure of contemporary science', Neville Hodgkinson, Fourth Estate, 1996, page 375). Since 1989, detection of a 24,000 molecular weight protein (p24) in cell cultures, (T cells from persons presumed to be infected), or co- cultures, (of T cells from persons presumed to be infected, with T cells from normal individuals), has been used to quantify HIV in cells, "cellular viremia" (Masquelier et al., 1992). Detection of p24 in cultures of T cells from normal individuals with plasma from those presumed to be infected has been used to quantify HIV in plasma, "plasma viremia" (Coombs et al., 1989; Ho et al., 1989; Clark et al., 1991). There are many reasons why p24 cannot be used to quantitate or even detect the presence of "HIV infectious particles". There is ample evidence that the p24 protein is not HIV specific (Papadopulos-Eleopulos et al., 1993a).
One needs to examine carefully whether or not the rules of retrovirus isolation have not been carefully respected for HIV. These rules are: culture, purification of the material by ultracentrifugation, Electron Microscopic (EM) photographs of the material which bands at the retrovirus density, characterization of these particles and proof of the infectivity of the particles.
For Luc Montagnier of the Pasteur Institute that is not isolation. His understanding of isolation is "we 'passed on' the virus" by making a culture of the virus. He says, "For example Gallo said they have not isolated the virus...and we (Gallo et al.), we have made it emerge in abundance in an immortal cell line." But before making it emerge in immortal cell lines, we made it emerge in cultures of normal lymphocytes from a blood donor. That is the principal criterion. One had something one could pass on serially, that one could maintain. And characterised as a retrovirus not only by its visual properties, but also biochemically, RT [reverse transcriptase] activity which is truly specific of retroviruses. We also had the reactions of antibodies against some proteins, probably the internal proteins. I say probably by analogy with knowledge of other retroviruses. One could not have isolated this retrovirus without knowledge of other retroviruses, that's obvious. But I believe we have answered the criteria of isolation. Totally." So, his principal criterion is totally different from the standard internationally laid rules.
Technically, the first isolation based on the principal criterion of Luc Montagnier came from a culture and not from purification. In fact there was so little production of virus in his culture that it was impossible to see what might be in a concentrate of virus from a gradient. There was not enough virus to do that. He only saw some particles but they did not have the morphology typical of retroviruses. They were very different. Relatively different. He agrees that he did not purify or failed to purify. And, in spite of that he has always recognized that it was truly the cause of AIDS! The definite existence of any virus, including a retrovirus, can be proven only by isolating it. For nearly half a century retroviruses have been isolated by banding in density gradients. The procedures incorporated into this method, which are by no means perfect, were not followed by the researchers who claim isolation of the human immunodeficiency virus, HIV-1. And Luc Montagnier did not follow the "traditional...Pasteur rules".
What Luc Montagnier did is clearly stated in the 1983 paper entitled "Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS)", where Montagnier and his colleagues reported the "isolation" of their "HIV" strain, cells obtained from a lymph node biopsy of a gay man with lymphadenopathy (lymphadenopathy syndrome [LAS]) were put in culture with PHA, IL-2 and antiserum to human interferon. The latter had previously been shown in mice to lead to "increased retrovirus production by a factor of 10 to 50". After 15 days Reverse Transcriptase activity was detected using the synthetic primer- template A(n).dT15. The reverse transcription of A(n)dT15 was considered proof that a retrovirus was present in the lymph node cells. The finding of the same activity in the supernatant of a co-culture of the same cells with lymphocytes from a healthy individual was considered proof that the retrovirus could be transmitted. Reverse transcriptase (RT) was first discovered as an essential catalyst in the biological cycle of retroviruses. However, in the past years, evidence has accumulated showing that RTs are involved in a surprisingly large number of RNA-mediated transcriptional events that include both viral and non-viral genetic entities!
Then came the genie that ravaged social lives. Somehow, without proof that they are coded by "HIV DNA", or they belong to a retrovirus-like particle, the following proteins, gp160/150, gp 120, gp45/40, p34/32, p24, p18/17 found either in cells, supernatants, or banding at 1.16 gm/ml in sucrose density gradients became known as the HIV proteins. In other words, contrary to all scientific reasoning, it was postulated that AIDS sera contain specific HIV antibodies and the proteins with which these antibodies react were defined HIV specific proteins. In 1985, Gallo and his colleagues, comparing the fourth open reading frame (ORF) of the "HIV DNA" which they called env-lor, with the env genes of other retroviruses, reported that "HIV" fourth open reading frame (ORF) was found to be identical to that of the protein present in the Western blot (41,000). Gallo claimed that the interaction of gp41 with antibodies found in AIDS patient sera is proof that gp41 is coded by the "HIV genome", and that both gp41 and the antibodies are specific to a retrovirus. In contrast, when Gallo and his colleagues reported the presence in humans of antibodies, in 1981, to what he now calls the first human retrovirus, HTLV-I, they described the finding of antibodies to a "major internal structural protein (p24) of HTLVCR" and claimed that such antibodies were "specifically directed at HTLVCR proteins and not at cell-specific determinants. This means that the immunological reactions are not those reported in human sera against animal virus glycoproteins which, lacking virus specificity, are directed against the carbohydrate residues of the glycoprotein". If the claim by Gallo that the interaction of gp41 with antibodies found in AIDS patient sera is proof that gp41 is coded by the "HIV genome" why is it that he has never been able to isolate the virus and purify it and reinfect other cells and produce the pathogenic effects of HIV?
In 1980, two research groups, one from the Laboratory of Cellular and Molecular Biology, National Cancer Institute and the other from the Laboratory of Viral Oncology, Memorial Sloan-Kettering Cancer Center, using the "viral glycoproteins", found that the antibodies present in human sera which reacted with these proteins were "directed against carbohydrate structures" and concluded that "The results are consistent with the idea that the antibodies in question are elicited as a result of exposure to many natural substances possessing widely cross-reacting antigens and are not a result of widespread infection of man with replication competent oncoviruses".
Before 1987 a positive ELISA with or without a WB was considered proof of HIV infection. However, it was realized that many individuals (4000/6000 [67%] in one study who had a positive ELISA did not test positive when the WB was performed. This was interpreted as evidence that the WB was more specific than the ELISA. By 1989, researchers from New York showed that in Western Blot (WB) analyses, "the components visualized in the 120-160 kDa region do not correspond to gp120 or its precursor but rather represent oligomers of gp41". It was also shown that the WB pattern obtained is dependent on many factors including temperature and the concentration of sodium dodecyl sulphate used to disrupt the "pure virus". Confusion over the identification of these bands has resulted in incorrect conclusions in experimental studies. Similarly, some clinical specimens may have been identified erroneously as seropositive. A postulate without scientific testing became a medical diagnostic laboratory tool that specialists used to “confirm” a positive diagnosis with the results of a Western Blot test in spite of the following language used in the test report - “Indicates possible infection by virus. Viremia may be present. Positive results are not diagnostic of AIDS. Biologic false positives still possible in some select cases. Follow up testing may be advised if clinical findings are discordant with test results.”
The serological diagnosis of HIV infection is usually made on the basis of the detection of circulating antibodies specific for viral antigens gp41, gp120 and gp160. A confirmed positive test [i.e. one or two ELISA tests, followed by a Western Blot] indicates that a person has been exposed to the virus and has mounted an immunologic response (serum antibodies). Normally, this should mean that after such an immunological response, the person is protected from the virus and is not proof of a progressing disease that will ravage his immune system and naturally this test does not indicate whether the person currently harbors the virus. So, AIDS is diagnosed worldwide if antibody against (!) HIV, rather than HIV, is detected in a patient along with any of the CDC’s 26 diseases. Since 1992 even low T-cell counts are diagnosed as a condition, termed “HIV/AIDS”.
A disclaimer printed on the packet insert in the ELISA test kit is as follows: "… the ELISA was designed to be extremely sensitive. As a result, non- specific reactions may be seen in samples from some people, who, for example, due to prior pregnancy, blood transfusion, or other exposure, have antibodies to the human cells or media in which the HIV-1 is grown for manufacture of the ELISA. Because of these and other nonspecific reactions, it is appropriate to investigate specimens found to be reactive on ELISA in a manner that gives improved predictability that HIV-1 antibody, in fact is present. Abbott Labs test kit instructions also contain the disclaimer: "There is no recognized standard for establishing the presence or absence of HIV-1 antibody in human blood" (Abbott, 1997) . 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. Persons having antibodies to laboratory chemicals such as trinitrophenyl may also show false positive results. Suddenly many healthy people were tested seropositive that stigmatized their very existence from the scare that "HIV was the probable cause of AIDS" which very quickly cascaded into "HIV was the
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