Sunday, October 23, 2011


by Beldeu Singh

It was big news in the mainstream media. A group of Chimpanzees had been locked up in metal cages for 30 years. They were kept by a firm that bought them that had the aim to find a vaccine to combat AIDS. The chimps were thought to be natural subjects because chimps share 99 per cent of the genome of man. Several years ago, the giant American pharmaceutical company Baxter took over the Austrian laboratory, and immediately announced it had no intention of continuing the testing program. “They suffered terrible cruelties in the years that followed, including being injected with the HIV virus. Hooked up to machines and pumped full of chemicals, they were truly prisoners of utter despair. With no stimulation, no nurturing love and no hope, many were driven to the brink of madness and beyond.”

What made the news and turned it into headlines? “Their ordeal finally ended on Tuesday when the 38 surviving chimps were released into a £3million sanctuary in Austria, allowing them to feel the nurturing contact of their fellow chimps after years of being separated by bars and bullet-proof glass.” Certainly a celebration but they missed the real news created by the laboratory to find a vaccine fir AIDS by injecting the so called HIV into the chimps but the chimps did not develop full-blown AIDS and they failed to find the vaccine. The failure to find a vaccine ought, rightly, to be the correct and the more exciting headline.
The news report said that “some chimpanzees were infected with the HIV virus. Of course, they became HIV positive. But none of them, not here in Austria or anywhere else in the world, developed full-blown Aids. Therefore, the program was useless. It achieved absolutely nothing.”
To get to the bottom of the matter embedded in this news, one has to grasp a number of issues as follows:-
  1. Why Dr. Gallo uses supernatants and not isolates?
  2. How do you do a clinical study comprising AIDS patients and HIV infection when the test kits carry a disclaimer stating that the test kits cannot be used to diagnose and treat AIDS and to use a confirmatory test?
  3. Why there are a large number of false positives with tests using these test kits, including people recovering from malaria and flu?
  4. Why do the HIV test kits test for p24, the significance of which is not known?
  5. What is the real role of gp120 in the infection process and in immune-suppression?
  6. Why give toxic drugs as medication to AIDs patients that suppress the immune system or are “toxic by inhalation” and “can cause the same symptoms as AIDS”?
  7. What is the treatment for drug-induced AIDS? More of the toxic medication?
  8. If AIDS is caused by a virus, why is there a latency period?
The claims regarding isolates of HIV appears false and upon close scrutiny may fall into the category of scientific fraud. Although during 1982 and much of 1983, the LTCB scientists' efforts to isolate and grow the AIDS virus failed again and again, Dr Gallo, in particular, repeatedly asserted that the first HIV isolates were obtained at the LTCB in late 1982-early 1983. "The first HTLV-III isolates were obtained in this laboratory in November 1982, and HTLV-III was subsequently isolated from approximately 100 patients with AIDS or ARC or from healthy individuals at risk for AIDS" (Gallo et al., in AIDS: Etiology, Diagnosis, Treatment and Prevention," 1985, p. 34). A practical approach is to infect a cell culture with virus obtained from supernatants in order to harvest an isolate. The term virus isolate refers to any particular virus culture that is recognizable as a biological entity that possesses some unique phenotypic properties that remain stable under natural conditions such as infecting a particular host and causing a particular disease or having antigenic properties. Variants may possess unique structural and genome sequence properties that are related to its antigenicity. So, an isolate constitutes stable replicating lineages that remain distinct over time and can be used to infect cells to observe their infectivity. The infectivity is neutralized by its specific antibodies and not by antibodies directed to other serotypes. In AIDS research, unfortunately, real isolates were not used and have never been obtained. Only supernatants were obtained and used but were referred to as “isolates.”
In 1890, Robert Koch described the basic rules that scientists use to determine if an infectious organism causes a specific disease. These four rules are called the "Koch's postulates." This process constitutes the scientific “Gold Standard”.  These criteria are:-
A.    The virus must be found in people with the disease and be absent in people without the disease.
B.    The virus must be able to be grown from tissues or other specimens from the infected individual in the laboratory and grown in a culture.
C.     The disease must be reproduced when this pure culture is introduced into a healthy host or when the virus is harvested from this pure culture and introduced into a susceptible healthy host.
D.    The virus must again be obtained from the experimentally infected host and grown in a culture.
According to Gallo et al, "the first HTLV-III isolates were obtained in this laboratory in November 1982, and HTLV-III was subsequently isolated from approximately 100 patients with AIDS or ARC or from healthy individuals at risk for AIDS" (Gallo et al., in AIDS: Etiology, Diagnosis, Treatment and Prevention," 1985, p. 34).

In August 1985, the "early isolates" claim was formally announced at the Proceedings of the National Academy of Sciences (PNAS). It was claimed that, "since the fall of 1982, independent isolates of HTLV-III have been obtained in this laboratory ... from 101 AIDS and ARC patients and healthy donors at risk for AIDS" (Salahuddin et al., PNAS, 82, pp. 5530-34). They stated precisely how they obtained and identified and defined their isolates for purposes of this PNAS paper:

"The minimum criteria used to identify new HTLV-III isolates were (i) release of particulate, Mg2+-requiring, viral reverse transcriptase into cell culture supernatant fluids...; (ii) transmission of virus to cultures of normal human peripheral blood mononuclear cells or to permissive T-cell lines with resulting characteristic cytopathic effects and release of virus ...; and (iii) detection of HTLV-III proteins by indirect immunofluorescence assays using virus-specific monoclonal antibody ... or hyperimmune sera ...".

In the same paper, they state that "All 101 virus isolates were classified as members of the type-III subgroup of HTLV based on their immunological reactivity with specific monoclonal antibody or hyperimmune antisera and by their cytopathic effect on normal peripheral blood mononuclear cells in vitro." In other words, according to Salahuddin et al., each and every one of their 101 isolates "since the fall of 1982" had been tested and found reactive with HIV-specific reagents. But there were three fundamental problems with these claims, as follows:-

 (a) no laboratory data have ever been produced to substantiate that "101" isolates, still less than the "over 200" claimed elsewhere by Dr. Gallo (9/23/85 Gallo-to-Fischinger memorandum) met the criteria specified in the PNAS paper, And

 (b) there is no evidence that any so-called "early isolates," particularly any isolate dating from the “fall of 1982” or early 1983 were ever tested by HIV-specific reagents, although, Dr. Gallo articulated the claim that once he had developed HIV-specific reagents, particularly the hyperimmune rabbit antiserum, he used the reagents to analyze and type archived samples, samples that he dated as early as 1982.

 (c) There was only particulate matter released in the supernatant fluids.
It was also claimed that "By December (1983) substantial quantities [of virus] were being grown, and soon afterward reagent production was underway. With reagents in hand, we could go back and identify the many stored viral isolates. Initial testing showed that the 48 isolates from AIDS patients or members of risk groups were of the same type" (p 50).
The 48-isolate claim and the companion claim that very early LTCB samples had been typed with HIV-specific reagents actually became a part of the settlement agreement, via their inclusion in a "Chronology of AIDS Research." The "Chronology," published by Montagnier and Gallo as a "Commentary" in Nature in April of 1987, was identified as "part of the agreement between the U.S. and French AIDS research groups" (Nature, 326, April 2, 1987; p. 435).
Not all members of the scientific community are aware of the "critical published facts" cited in this "official" chronology including the following:
  1. "May 1984. Gallo's group (1984) reports ... (2) 48 virus isolations ... The use of anti-p24 hyperimmune sera proves that the 48 isolates belong to the same kind of virus" (op cit., p. 436).
  2. In a 1988 Scientific American article, also coauthored by Gallo and Montagnier, the claim was repeated - "The first reagents for specifically typing this virus were rapidly made. Employing those reagents, it was shown that 48 isolates obtained beginning in early 1983 from AIDS patients and people in risk groups were all the same type of virus, which was called HTLV-III on the American side" (259, October 1988, p. 44).
  3. After developing the “HIV viral specific reagents” they went back to identify the “many stored isolates” instead of using these viral-specific reagents” to test for the virus upon harvesting it from re-infected normal peripheral blood mononuclear cells in vitro and in lab animals, which is a critical procedure in order to establish infectivity.
The initial work of Dr. Gallo and Montagnier is obviously flawed as seen from the above and in particular because of the fact that their reagents are not viral specific and are obviously not based on their immunological reactivity with specific monoclonal antibody – they do not test for viral-specific antibody, based on the evidence of a large number of false positives and their own evidence that it tests for concentration of p24 rather than the presence or absence of antibodies specific to a virus. The public must understand that if the reagents are indeed viral-specific, they will only indicate the presence or absence of the virus.
Since many viruses do not cause illness in all infected individuals as they may survive under conditions of established homeostasis, the Koch postulates may not apply in a classic manner. The human body is thought to manage a multitude of highly complex interactions to maintain balance or return systems to functioning within a normal range. However, this process may not be due to an actively managed process through specific biochemical processes. It is managed inadvertently through limitations in critical nutrient supply such as vitamin B12 that is required in protein synthesis or for the synthesis of genetic molecules for their growth and replication. A limited supply or availability tends to curtail the replication and proliferation of the microorganisms that are dependent on such micronutrients, especially those not produced by cells of the body. An inability to maintain homeostasis may lead to death or a disease, a condition known as homeostatic imbalance. Furthermore, is the fact that an infection with the same virus may lead to markedly different disease conditions. This is due to the fact that viral toxins cause inflammation or loss of cell-membrane integrity (or both), at the cellular level, in cells of different tissues in the body. The herpes simplex viruses-1 and -2 (HSV-1 and HSV-2) are human pathogens capable of infection and spread in a number of human cell types, with establishment of latent and recurrent infections.
Infectious diseases remain a major cause of death, disability, and social and economic disorder for millions of people throughout the world. Prevention and treatment strategies for infectious diseases derive from a thorough understanding of the complex interactions between specific viral or bacterial pathogens and the human (or animal) host. Just as glycans are major components of the outermost surface of all animal and plant cells, so too are oligosaccharides and polysaccharides found on the surface of all bacteria and viruses. Thus, most (if not all) interactions of microbial pathogens with their hosts are influenced to an important degree by the pattern of glycans and glycan-binding receptors that each expresses. This holds true at all stages of infection, from initial colonization of host epithelial surfaces, to tissue spread, to the induction of inflammation or host-cell injury that results in clinical symptoms (Victor Nizet and Jeffrey D Esko, 2009, Essentials of Glycobiology. 2nd edition, Chapter 39: Bacterial and Viral Infections, Cold Spring Harbor (NY), Bookshelf ID: NBK1952 PMID: 20301271).
The toxins and microbial molecules responsible for disease manifestations are known as virulence factors. Adherence to skin or mucosal surfaces is a fundamental characteristic of the normal human microflora and also an essential first step in the pathogenesis of many important infectious diseases. Most microorganisms express more than one type of adherence factor or “adhesin.” Pathogenic strains of Salmonella produce pili that facilitate adherence to human intestinal cell mucosa, thereby causing food poisoning and infectious diarrhea. In other cases, a surface-anchored protein (afimbrial adhesin) expressed by the bacteria represents a critical colonization factor (Figure 39.3b). The filamentous hemagglutinin (FHA) of Bordetella pertussis promotes strong attachment of the bacteria to the ciliated epithelial cells of the bronchi and trachea, triggering local inflammation and tissue injury that produces the “whooping cough” syndrome.  In a number of cases, the key adhesive factor is an assembly of protein subunits that project from the bacterial surface in hair-like threads known as pili or fimbriae (ref: Victor Nizet and Jeffrey D Esko, 2009, Essentials of Glycobiology. 2nd edition, Chapter 39: Bacterial and Viral Infections, Cold Spring Harbor (NY), Bookshelf ID: NBK1952 PMID: 20301271). Different viruses producing similar surface-anchoring proteins may produce similar symptoms. Hence, proving causation is not always easy, but at least, it is important to show the micro-organism associated with the disease condition or health problem.
The allergens produced by microparasites are also pathogenic factors and may have glycan-binding capacity or surface-anchoring proteins to trigger local inflammation resulting in a varied host of factors ranging from varicose veins to psoriasis and immune-suppression when they bind to receptors on cells of the immune system and/or infect then during the trophozoites stage in the life cycle.
In certain cases, the viral infection may not produce a disease condition as their replication may be severely curtailed by a lack of a particular nutrient in the cells of a culture or the animal model may not be suitable or due to a lack of specific receptors for the virus to attach. Again, in such cases the Koch postulates may not apply in a classic manner but there are other methods are sensitive and are fundamentally sound but modern versions of the basic notion put forth in the Koch postulates. Hepatitis (plural hepatitides) is a medical condition defined by the inflammation of the liver and characterized by the presence of inflammatory cells in the tissue of the organ (Online Etymology Dictionary). The condition can be self-limiting (healing on its own) or can progress to fibrosis (scarring) and cirrhosis, depending on whether or not the body can resolve or otherwise reduce the inflammation.
The application of nucleic acid-based methods of microbial identification through polymerase chain reaction and high-throughput sequence analysis have revealed a great deal about microbes that are associated with pathology or disease, but proving causation has become even more difficult as the number of uncultivable viruses rapidly multiplies. Nucleic acid based detection methods are so sensitive that they detect small numbers of viruses that may occur in the absence of disease. The use of these new methods have lead to revised versions of Koch’s postulates that are fundamentally sound: both hepatitis C virus and human papillomaviruses were convincingly shown to be agents associated with hepatitis and cervical cancer, respectively, long before methods were developed for propagation of the viruses in cell culture. The revised and modern version of the Koch’s postulates for the 21st century as suggested by Fredricks and Relman are as follows (Fredericks DN, & Relman DA, 1996, Sequence-based identification of microbial pathogens: a reconsideration of Koch’s postulates. Clinical microbiology reviews, 9 (1), 18-33 PMID: 8665474):
  1. A nucleic acid sequence belonging to a putative pathogen should be present in most cases of an infectious disease. Microbial nucleic acids should be found preferentially in those organs or gross anatomic sites known to be diseased, and not in those organs that lack pathology.
  2. Fewer, or no, copy numbers of pathogen-associated nucleic acid sequences should occur in hosts or tissues without disease.
  3. With resolution of disease, the copy number of pathogen-associated nucleic acid sequences should decrease or become undetectable. With clinical relapse, the opposite should occur.
  4. When sequence detection predates disease, or sequence copy number correlates with severity of disease or pathology, the sequence-disease association is more likely to be a causal relationship.
  5. The nature of the microorganism inferred from the available sequence should be consistent with the known biological characteristics of that group of organisms.
  6. Tissue-sequence correlates should be sought at the cellular level: efforts should be made to demonstrate specific in situ hybridization of microbial sequence to areas of tissue pathology and to visible microorganisms or to areas where microorganisms are presumed to be located.
  7. These sequence-based forms of evidence for microbial causation should be reproducible.
This new Fredericks-Relman version must now be applied to the HIV, especially in clinical studies.
Dr. Gallo is on record to have found his HIV, not in most of the AIDS patients, but in only 40% of the AIDS patients.  It was claimed that the HIV targets cells of the immune system, attaches to these cells and bores a hole in the cell surface to penetrate the cell for infection and then a budding process is supposed to take place. Such a process does not occur when the infective agent is micro-particulate in nature that does not replicate. Hence this budding process has never been observed and documented.
“The genome of HIV contains only three major genes (env, gag, and pol) that direct the formation of the basic components of the virus. Glycoprotein products of the env gene include an envelope precursor protein gp160 (which undergoes proteolytic cleavage to form the outer envelope glycoprotein gp120 that is responsible for the cellular tropism of the virus) and transmembrane glycoprotein gp41 (which catalyzes fusion of HIV to the target cell’s membrane). The first step in HIV infection involves the high-affinity attachment of the CD4-binding domains of gp120 to CD4, a receptor present on certain T cells, macrophages, dendritic cells, and microglial cells. Once gp120 is bound to the CD4 protein, the HIV envelope undergoes a structural change, exposing additional binding domains of gp120 that interact with a cell-surface chemokine coreceptor (CCR5 or CXCR4). This more stable two-pronged attachment allows gp41 to penetrate the cell membrane, bringing the virus and cell membranes in close approximation for fusion and subsequent entry of the viral capsid containing the replication enzymes reverse transcriptase, integrase, and ribonuclease into the cell. Sulfated tyrosine residues contribute to the binding of CCR5 to gp120/CD4 complexes and to the ability of HIV-1 to enter cells. The differences in chemokine coreceptors present on cells can also explain how different strains of HIV may infect cells selectively. Strains of HIV known as T-tropic strains selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes, whereas M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages.” (see:  Victor Nizet and Jeffrey D Esko, 2009, Essentials of Glycobiology. 2nd edition, Chapter 39: Bacterial and Viral Infections, Cold Spring Harbor (NY), Bookshelf ID: NBK1952 PMID: 20301271).
How does gp160 undergo “proteolytic cleavage” to form gp120 and gp41 which is a very specific cleavage unless the HIV produces a specific enzyme for such purpose? And why would the binding of gp120 to the chemokine receptors cause a structural change in the glycoprotein (gp120) in favor of the virus? They say that gp41 is a product of proteolytic cleavage whereas Dr. 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 that case, there should be no false positives.

“The precise cause of the CD4+ T-cell abnormalities seen in HIV infection is not now known. Abnormalities occur in both the presence and the absence of direct infection of the CD4+ T cell (for review, see Rosenberg and Fauci 1989a, 1992). Direct killing may deplete certain functional subsets of CD4+ T cells eliminating that particular immune function. Even when an infected cell is not killed, its function may be compromised. The cell surface expression of the CD4 receptor in infected CD4+ T cells is down-modulated as the HIV gp120 molecules produced during viral replication bind to cytoplasmic CD4, forming intracellular gp120-CD4 complexes” (Retroviruses,  1997, Immunopathogenic Mechanisms of HIV Infection : Mechanisms of CD4+ T Lymphocyte Dysfunction, Coffin JM, Hughes SH, Varmus HE, editors: Bookshelf ID: NBK19451). The HIV was originally made out to be a virulent pathogen that targets the cells of the immune system and HIV infection killed those cells but more and more researchers now agree that an “infected” cell may not be killed but its role may be suppressed.

The AIDS posse, including Luc Montagnier says that “there is evidence for a negative effect of HIV on signal transduction. In vitro, the crosslinking of CD4 molecules that occurs when gp120 is bound in the presence of anti-gp120 antibodies causes suppression of T-cell activation” (Mittler and Hoffmann 1989). Anti-gp120 antibody-coated CD4+ T cells have been detected in HIV-infected individuals, suggesting that soluble gp120 can bind CD4 molecules in vivo and HIV gp120-induced T-cell anergy could occur (Amadori et al. 1992:(cf: Retroviruses, 1997, Immunopathogenic Mechanisms of HIV Infection: Mechanisms of CD4+ T Lymphocyte Dysfunction, Coffin JM, Hughes SH, Varmus HE, editors: Bookshelf ID: NBK19451). So, while the AIDS posse claims that the key molecule or molecular fragment is gp120, the HIV test kit manual says that they are detecting concentrations of p24, the significance of which is not known” and the HIV test result is based on the concentration of p24 instead of the presence or absence of a specific antibody. So, who is fooling whom? The manufacturers of those test kits were smart enough to print a disclaimer which says that these test kit cannot be used to diagnose and treat AIDS.
While more and more researchers claim that gp120 causes suppression of T-cell activation, in two papers (in 1991 & 1993) Luc Montagnier, wrote that in HIV-infected patients, the loss of CD4+ cells is associated with lymphocyte activation, but this activation does not result in lymphocyte activation but in programmed cell death called apoptosis. It may not be programmed cell death as gp120 is not known to alter the genetic programming. The mechanism may one that involves the cytotoxic T cells and leukocyte activation that triggers excess cytokine production that kills the cells secreting the excess cytokines. Cytotoxic T cells   (TC cells, or CTLs) destroy tumor cells and cells infected with viruses or gp120 attachment to receptors in certain cells, like the CD4 cell may trigger excess production of interleukins that kill them. It appears that exposure to a specific antigen, mitogen, cytokine, chemokine, cellular ligand can alter the morphology and behavior of a lymphocyte while a soluble factor such as gp120 can alter its internal biochemistry triggering an over-production of interleukins. Cytotoxic T cells may be acting against cells in which the cell junctions have become impaired by gp120 attachment to receptors, allowing viruses to gain easy entry into them. Hence viral loads can be used to predict disease progression in only 2-6% of patients with immune suppression.
Red White Blood cells.jpg
Fig 1. Scanning electron micrograph of T lymphocyte (right), a platelet (center) and a red blood cell (left)
Wikipedia: T-cell
“Unbalanced interleukin network and elevated IL-6 synthesis point to mechanisms of immunoglobulin overproduction in children with perinatal human immunodeficiency virus-type 1 (HIV-1) infection. Children with high IgE levels had higher spontaneous IL-6 synthesis (1337 +/- 138 pg/mL) compared with those without high IgE levels (861 +/- 194 pg/mL; P < .001). By contrast, spontaneous IL-6 synthesis was similar in children with or without high IgG, IgA, or IgM levels. Decreased PHA-stimulated IL-2 synthesis, low CD4+ lymphocyte counts, elevated HIV-1 RNA copy numbers and severe disease correlated with high IgE (but not IgG, IgA, and IgM) levels. IgG, IgA, and IgM levels correlated with each other, but not with IgE levels (de Martino M, Rossi ME, Azzari C, Chiarelli F, Galli L, Vierucci A, Interleukin-6 synthesis and IgE overproduction in children with perinatal human immunodeficiency virus-type 1 infection, Ann Allergy Asthma Immunol. 1999 Feb;82(2):212-6). Overproduction of certain interleukins is associated with low CD4 lymphocyte counts.
IgM is important to clear microbes and other bio-particles, small size-late apoptotic cells and blebs/microparticles (Litvack ML, Post M, Palaniyar N (2011) IgM Promotes the Clearance of Small Particles and Apoptotic Microparticles by Macrophages. PLoS ONE 6(3): e17223). On the other hand, upon first contact with allergen, differentiation of naïve Th0 cells into Th2 cells and stimulation of B cells to produce IgE and IgG1 are regulated by IL-4. Further allergen exposure leads to cross-linking of allergen by IgE bound to the surface of mast cells and basophils (H. Metzger, The receptor with high affinity for IgE. Immunol. Rev.,  125  (1992), p. 37–48)[101] H. Metzger, The receptor with high affinity for IgE. Immunol. Rev.,  125  (1992), pp. 37–48. | View Record in Scopus | | Full Text via CrossRef. Dendritic cells (DC) play a key role in innate and adaptive immunity. They have a regulatory effect on the production of Immunoglobulins. They are professional antigen-presenting cells (APC) and able to phagocytose antigens, viruses, bacteria or—at some extent—microparticles. Microparticles were efficiently phagocytized by DC or macrophages in vitro and in vivo. Of particular interest is the capability of particulate vaccine delivery systems to invoke cell mediated immune responses. Both more efficacious vaccines for existing indications and novel products for new indications appear to be achievable. Dendritic cells produce interleukins – IL-6 and IL-17 (M. Maizels, Stephen M. Anderton and Andrew S. MacDonald, O'Connor, Dimitrios, Zienkiewicz, Henry J. McSorley, Rick, Georgia Perona-Wright, Stephen J. Jenkins, Richard A. A Pivotal Role for CD40-Mediated IL-6 Production by Dendritic Cells during IL-17 induction in Vivo, J Immunol 2009;182;2808-2815). Dendritic cells can express the high-affinity IgE receptor (FcϵRI), which, in the presence of specific IgE, facilitates the uptake of allergen, leading to increased activation of allergen-specific T cells (Judith A. Holloway,Affiliations
·       Stephen T. Holgate,Affiliations
·       Amanda E. Semper, Expression of the high-affinity IgE receptor on peripheral blood dendritic cells: Differential binding of IgE in atopic asthma, The Journal of Allergy and Clinical Immunology, 2001). The high Il-6 levels and IgE levels but not high IgM levels indicate that the innate immune response is not mediated against microbes but allergenic particles in patients indentified by HIV tests and classified as HIV patients. These allergenic particles originate from secretions of microparasites.
If "HIV" is as an exogenous unique retrovirus that can be actually found in true isolates, why would a Hepatitis B vaccine (Lee, D, Eby W, Molinaro, G. HIV false positivity after Hepatitis B vaccination. Lancet 339: 1060, 1992), or flu vaccine (Simonsen L, Buffington J, Shapiro CN, et al. Multiple false reactions in viral antibody screening assays after influenza vaccination. Am J Epidemiol 141:1089-1096, 1995; Christian, P. Erickson, Todd McNiff, Jeffrey D. Klausner. Influenza Vaccination and False Positive HIV Results, New England Journal of Medicine, Number 13 , Volume 354:1422-1423), cause about 2% false positives?

Christine Johnson, a researcher and author, compiled a long list of conditions documented in scientific literature to cause positives on HIV tests, and provides references for each condition. He cites 63 research papers by over 100 scientists. The list - Anti-carbohydrate antibodies; Naturally-occurring antibodies; Passive immunization: receipt of gamma globulin or immune globulin (as prophylaxis against infection which contains antibodies); Leprosy; Tuberculosis; Mycobacterium avium; Systemic lupus erythematosus; Renal (kidney) failure; Hemodialysis/renal failure; Alpha interferon therapy in hemodialysis patients; flu vaccination; Herpes simplex I; Herpes simplex II; upper respiratory tract infection (cold or flu); Recent viral infection or exposure to viral vaccines; Pregnancy in multiparous women; Malaria; High levels of circulating immune complexes; Hypergammaglobulinemia (high levels of antibodies); False positives on other tests, including RPR (rapid plasma reagent) test for syphilis; Rheumatoid arthritis; Hepatitis B vaccination; Tetanus vaccination; Organ transplantation; Renal transplantation; Anti-lymphocyte antibodies; Anti-collagen antibodies (found in gay men, haemophiliacs, Africans of both sexes and people with leprosy); Serumpositive for rheumatoid factor, antinuclear antibody (both found in rheumatoid arthritis and other autoantibodies); Autoimmune diseases; Systemic lupus erythematosus, scleroderma, connective tissue disease, dermatomyositis Acute viral infections, DNA viral infections; Malignant neoplasms (cancers); alcoholic hepatitis/alcoholic liver disease; Primary sclerosing cholangitis; Hepatitis; "Sticky" blood (in Africans); Antibodies with a high affinity for polystyrene (used in the test kits); Blood transfusions, multiple blood transfusions; Multiple myeloma; HLA antibodies (to Class I and II leukocyte antigens); Anti-smooth muscle antibody; Anti-parietal cell antibody; Anti-hepatitis A IgM (antibody); Anti-Hbc IgM; Administration of human immunoglobulin preparations pooled before 1985; Haemophilia; Haematologic malignant disorders/lymphoma; Primary biliary cirrhosis; Stevens-Johnson syndrome; Q-fever with associated hepatitis; Heat-treated specimens; Lipemic serum (blood with high levels of fat or lipids); Haemolyzed serum (blood where haemoglobin is separated from the red cells); Hyperbilirubinemia; Globulins produced during polyclonal gammopathies (which are seen in AIDS risk groups); Healthy individuals as a result of poorly-understood cross-reactions; Normal human ribonucleoproteins; Other retroviruses; Anti-mitochondrial antibodies; Anti-nuclear antibodies; Anti-microsomal antibodies; T-cell leukocyte antigen antibodies; Proteins on the filter paper ; Epstein-Barr virus; Visceral leishmaniasis and Receptive anal sex. “Sticky” blood has been noted in people with micro-parasite infection. The “stickiness” is due to the effects of the allergens secreted by the microparasites on the cell membranes of the RBCs.

So, the HIV test is not valid and hence the disclaimer on these tests kits, as properly advised by their lawyers. If so, how do you carry out other HIV related experiments? How do you identify the HIV-infected population for study and for conducting clinical trials?
The HIV GP160 protein exists only in the intracellular domain, where it is cleaved into GP41 and GP120 oligomers. Since GP160 itself is not present in mature HIV virions, 5 GP160 proteins and antibodies against these proteins should be absent not only from the Western blot assays but also in most cases from the serum of HIV-infected patients (Christian, P. Erickson, Todd McNiff, Jeffrey D. Klausner. Influenza Vaccination and False Positive HIV Results, New England Journal of Medicine, Number 13 , Volume 354:1422-1423, 2006). This study raises the question on the source of gp120 and gp-proteins. Are they actually from a viral coat or produced during HIV viral replication or produced in the body during conditions of oxidative stress?
Palamara et al, investigated the effect of glutathione on the replication of human immunodeficiency virus (HIV) in chronically infected macrophages, a known reservoir of the virus in the body (AIDS Res Hum Retroviruses 1996 Nov 1;12(16):1537-41) and found that exogenous GSH strongly suppresses the production of p24 protein. That is an interesting link between glutathione (GSH), an antioxidant enzyme produced in the body and p24. The higher the amount of exogenous GSH the lower the amount of p24 the body will produce. Similarly if the patient gets bio-available selenium which is essential to the production of glutathione in the body the level of p24 will decline. So, is the p24 part of the body’s antioxidant defense mechanism and an indication of low glutathione levels and oxidative stress or is it an antigen that indicates a viral infection or is it an antibody?

Like Montagnier, Robert Gallo and his colleagues did not publish electron micrographs to show that their “purified” virus contained retrovirus-like particles.  Unlike Montagnier et al who considered the protein of molecular weight 24,000 (p24) as being the characteristic HIV proteins, Gallo et al considered a protein of molecular weight 41,000 (p41), which is the molecular weight of actin, as the most specific HIV protein.  The only proof they gave for this was its banding at the density of 1.16gm/ml and reaction with the sera of AIDS patients. How did Dr. Gallo use this as proof of a pure virus particle? He relied on a Franco-German study published in 1997. In that study, the authors, which included Hans Gelderblom, pointed out that although the 1.16gm/ml band, which is used for “biochemical and serological analyses”, is “considered to contain a population of relatively pure virus particles, … and in none of the studies has the purity of the virus preparation been verified” (Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ. Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations, Virology 1997; 230:125-133).  However, by 1997, ample evidence existed which showed that the 1.16gm/ml band contains many cellular proteins including actin and myosin, the latter also an ubiquitous protein which has two light chains of molecular weight 24,000 and 18,000.  Evidence also exists that AIDS patients have antibodies to both actin and myosin.(ref; Perth Group, July 2000, NIH Antibodies: Matsiota P, Chamaret S, Montagnier L. Detection of Natural Autoantibodies in the serum of Anti-HIV Positive-Individuals. Annales de l'Institut Pasteur Immunologie, 1987; 138:223-233).

Proof of contamination proves that the particular band does not contain “purified viruses.” Two papers published in Virology in 1997 with the first electron micrographs of “purified HIV” obtained by banding the supernatant of “infected” cultures in sucrose density gradients.  One of the studies was by researchers from the AIDS Vaccine Program SAIL, National Cancer Institute–Frederick Cancer Research and Development, Frederick, Maryland, USA and the other by researchers from France and Germany (Bess JW, Gorelick RJ, Bosche WJ, Henderson LE, Arthur LO. Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations. Virology 1997; 230:134-144:     Gluschankof P, Mondor I, Gelderblom HR, Sattentau QJ. Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations, Virology 1997; 230:125-133: ref; Perth Group, July 2000, NIH Antibodies). The authors of both studies claimed their “purified” material contains retrovirus-like particles and in fact that they were HIV particles.  But they admitted that their material predominantly contained particles which were not viruses but “mock virus” that is “budding membrane particles frequently called micro-vesicles”.  Indeed, the caption to one of the electron micrographs of the “purified” HIV reads:  “Purified vesicles from infected H9 cells (a) and activated PBMC (b) supernatants." It does not read “purified HIV”.  In further experiments, the supernatants from non-infected cultures were also banded in sucrose gradients.  They claimed that the banded material from these cultures contained only micro-vesicles, “mock virus” particles, but no particles with the morphology of HIV. Dr. Gallo could have used these particles to infect normal cells in order to harvest the virus but this was not done or was not reported as such particulate matter in not infective. There is a big difference between “viral particles” or “viral glycoproteins” obtained from supernatants and isolates.

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." That explains why the HIV tests result in a so many false positives and the fact that the so called HIV specific antibody is not a protective antibody, which means that if scientists are looking a vaccine based on “viruses” in supernatants, as in the case of the freed chimps, any antibodies produced by such eliciting will have no protective value and cannot be used as vaccines and such vaccine research is futile. 

In 1988, researchers reported a contradictory observation to the findings of Christian P et al (2006) that a clone of the HUT78 cell line, chronically infected with the HIV-1 isolate HTLV-III451, has been demonstrated to secrete unprocessed HIV-1 envelope precursor protein gp160 as well as mature gp120 that formed high-affinity soluble complexes with the CD4 antigen (Kalyanaraman VS, Pal R, Gallo RC, Sarngadharan MG, A unique human immunodeficiency virus culture secreting soluble gp160, AIDS Res Hum Retroviruses. 1988 Oct;4(5):319-29) but they did not report finding gp40 or gp41. Other researchers, including Luc Montagnier, say that the proteolytic cleavage of the envelope glycoprotein precursor (gp160) is carried out by cellular protease converting it into the external gp120 and the transmembrane gp41 for complete activation of human immunodeficiency virus type 1 (HIV-1) (Maxime Moulard, Luc Montagnier, Elmostafa Bahraoui, Effects of calcium ions on proteolytic processing of HIV-1 gp160 precursor and on cell fusion, Volume 338, Issue 3, 7 February 1994, Pages 281-284). If a retrovirus has already infected the cell in which the envelope gp160 undergoes cleavage which are apparently secreted into the intracellular space, then these glycoproteins are not produced by their HIV but are cleavage products of viral coats in general, including the EBV followed by secretion of these cleavage proteins and the gp120 forms high-affinity complexes with chemokine receptors causing the production of cytokines that kill cells of the immune system in the vicinity of the cytokine-produce cells. However, this cleavage may not be a proteolytic cleavage produced by cellular protease at all but one that occurs in cells under oxidative stress and is caused by free radicals, which explains why these gp-protein fragments are found in intracellular spaces and are not produced during viral replication and that also explains why glutathione and antioxidant treatment decreases the level of these products and further explains why AIDS is not a typical sexually transmitted disease. Proteolytic cleavage by cellular protein indicates a period of co-evolution between the pathogen and host which is not the proven case.
These cleavage products might be coming from the Epstein - Barr virus (EBV).   The EBV resides as a persistent infection in human leukocyte antigen (HLA) class II+ B lymphocytes and is associated with a number of malignancies. The EBV lytic-phase protein gp42 serves at least two functions: gp42 acts as the coreceptor for viral entry into B cells and hampers T-cell recognition via HLA class II molecules through steric hindrance of T-cell receptor-class II-peptide interactions (Maaike E. Ressing et al, Epstein-Barr Virus gp42 Is Posttranslationally Modified To Produce Soluble gp42 That Mediates HLA Class II Immune Evasion, Journal of Virology, January 2005, p. 841-852, Vol. 79, No. 2). Hence, it may well be the case that the so called HIV may in fact be an ordinary retrovirus like the EBV, not a new virus.
Exposure of RAW 264.7 macrophages to JP, a cell permeant analog of phalloidin that increases and stabilizes polymerized actin in living cells, reduced the ability of RAW 264.7 macrophages to
phagocytose fluorescent Klebsiella by 50%. This indicates that increased actin polymerization is a potential mechanism explaining impairment of phagocytosis by oxidative stress and since AIDS is a condition caused by excess free radicals (in malnourished people) (see Philip J et al, Hyperoxia Impairs Antibacterial Function of Macrophages through Effects on Actin, American Journal of Respiratory Cell and Molecular Biology. Vol. 28, pp. 443-450, 2003), it quite clearly proves that oxidative stress on macrophages leads to increased actin polymerization and formation of prominent stress fibers and actin aggregates which could also occur in people recovering from malaria, influenza or in people suffering from chronic fatigue due to mitochondrial oxidative stress or ethanol toxicity or drug induced oxidative stress. This explains the large number of false positives using the HIV-tests in people recovering from malaria or flu and further proves that HIV tests are not HIV-specific. Immunoglobulins are also critical in the phagocytosis of actin polymers.
In mammals, binding of immunoglobulins (Igs) to foreign particles leads to the prompt clearance of those particles from the organism. Igs act as opsonins, molecules that render the particle they coat more susceptible to engulfment by phagocytic cells. Professional phagocytes such as neutrophils and macrophages tend to rapidly internalize and phagocytosize the opsonised particles (Robin C. May and Laura M. Machesky, Phagocytosis and the actin cytoskeleton, Journal of Cell Science 114, 1061-1077 © The Company of Biologists Ltd, p 1061-1075). This internalization is characterized by the dramatic, actin-dependent extension of the plasma membrane around the particle and is followed by secondary activity, such as the production of superoxide and the release of inflammatory cytokines from the phagocyte (Roitt, I. M. 1994, The basis of immunology. In Essential Immunology. Blackwell Scientific, Oxford) as shown in Fig 2. The secondary activity is the cause if immune suppression especially when antioxidant levels (eg L-ascorbic acid and glutathione) are low in such cells .

Fig. 2.  The scanning electron micrograph shows an IgE-opsonised zymosan
particle being engulfed by an RBL-2H3 cell, an FceR-mediated event. Note the dramatic protrusion of membrane around the particle. Image kindly provided by Philippe Montcourrier and Philippe Chavrier. (ref: Robin C. May and Laura M. Machesky).

Glyco-proteins have cleavage sites and can cleave at those sites under free radical action as free radicals rob electrons at bonds at these sites to weaken the bonds leading to breaking of the bonds to yield cleavage fragments that are subject to clearance by phagocytosis. Actin-binding protein, an ubiquitous actin in peripheral cytoplasm that links actin filaments to membrane glycoproteins may have a significant role to play in immune suppression when it links with cleaved glycol-proteins. Actin is a globular, roughly 42-kDa protein with many roles depending on its cross-linkages Thus, actin participates in many important cellular processes including muscle contraction, cell motility, cell division and cytokinesis, vesicle and organelle movement, cell signaling, and the establishment and maintenance of cell junctions and cell shape and in energy that is bio- available as one of its form (G-actin) binds to ATP for conversion to ADP for release of energy for use within the cell. Under oxidative stress, polymerized actin may link with cleaved glyco-proteins such as gp41 or gp42 affecting energy levels in the cell as well as compromising the integrity of the cell junctions that may allow viruses to enter the cells of the immune system and together it leads to an impairment of phagocytosis and immune suppression that opens the body to opportunistic infections. At this stage and when gp120 attaches to the chemokine receptors on leukocytes the T4 cells and lymphocyte count may decline.
According to HIV researchers, “one of the early hallmarks of HIV infection, prior to the profound depletion in CD4+ T cells, is the impairment of a variety of CD4+ T-cell functions including T-cell colony formation, autologous mixed lymphocyte reactions, expression of interleukin-2 (IL-2) receptors, and IL-2 production (for review, see Rosenberg and Fauci 1989a:cf: Retroviruses,  1997, Immunopathogenic Mechanisms of HIV Infection : Mechanisms of CD4+ T Lymphocyte Dysfunction, Coffin JM, Hughes SH, Varmus HE, editors: Bookshelf ID: NBK19451). If gp120 is the key factor in cell death by apoptosis of cells of the immune system that leads to a profound depletion of T4 cells during the early stage of HIV infection, the HIV must first enter the cells of an infected person and only then more gp120 is produced during viral replication in the infected cells. However, research in immunology reveals that oxidative stress alters the biochemistry in cells of the immune system upon cleavage of glycol-proteins by excess free radicals, namely gp120 and polymer actin and subsequent phagocytosis by cells that are low in antioxidants followed by a secondary process involving excess free radicals and cytokines that kills participating cells.
Current literature states that the so called HIV, most commonly uses CCR5 and/or CXCRA4 as a co-receptor to enter its target cells, as the molecules on the HIV enveloped cell wall can attach or bind to this receptor. And very recently, a Cornell University researcher and a consultant for The American Foundation for AIDS Research and a dozen doctors from around the nation, including three from Seattle, met last week in Philadelphia to discuss their research which focuses on CCR5, essentially a doorway HIV uses to enter cells. They are saying, there is a doorway, called CCR5, in the cell wall that is used by the HIV to enter cells. And gp120 is required for their HIV to gain entry into cells. Once inside the cells of the immune system, their HIV replicates and during this replication, more gp120 is produced. The question here is whether the gp120 is produced during HIV replication in cells or is the result of proteolytic cleavage by cellular protease or a cleavage caused by excess free radicals in the cells that have targeted retroviruses and EBV. The easy entry by viruses is gained through impaired cell junctions by gp120 and polymerized actins.
Lymphocyte activation results in the production of chemokines that target the invading pathogen. All chemokines have very small binding sites to enable them to play the role of binding into receptor sites on cell surfaces. Chemokine receptors are G protein-coupled receptors containing 7 transmembrane domains that are found on the surface of leukocytes. Approximately 19 different chemokine receptors have been characterized to date, which are divided into four families depending on the type of chemokine they bind; CXCR that bind CXC chemokines, CCR that bind CC chemokines, CX3CR1 that binds the sole CX3C chemokine (CX3CL1), and XCR1 that binds the two XC chemokines (XCL1 and XCL2). They share many structural features. In response to an infection, chemokines are produced to target the pathogen by activating the leukocytes but protozoa can produce molecules that mimic the host chemokines and can compete to bind to receptor sites on leukocytes to suppress their targeted response against the protozoa and can lead to immune suppression that is best eliminated by killing the microparasites by phytochemicals that work synergistically with natural antioxidants.
Toxoplasmic encephalitis, exacerbated by a compromised immune system, is a common AIDS complication (Cohen, B.A. (1999) Semin. Neurol. 19:201) and protozoal induced immune suppression may be largely responsible for the progress of AIDS in at least 50% of the AIDS population and it also explains its latency. Infection of T. gondii in mice causes depletion of CD4+ T-lymphocye (Luft BJ et al, 1993, Toxoplasmic encephalitis in patients with acquired immunodeficiency syndrome, N. England J. Med., 329:995-1000: DR Arora and B Arora, Medical Parasitology, 2nd Edition, CBS Publishers and Distributors, p87). It is the most common protozoa in AIDS patients and at 38% it corresponds to the 40% figure quoted by Dr. Gallo stated in his testimony in a South Australian Court that he found the “HIV” in only forty percent of AIDS patients - AIDS the percentage positive was 37.5%, for adult AIDS with Kaposi’s sarcoma, 30.2%, and for adult AIDS with opportunistic infections 47.6%’, at page 1300 : isolation of HIV from 48 out of 119 patients, that is, 40%, at p 1294, (see: The Gallo Files – HIV on Trial, © Copyright March, 2007 by Garlan) and is the most common cause intracerebral lesions in AIDS patients and is associated low CD4+ t-cell counts (see” Luft BJ and Remington JS, 1992, Toxoplasmic encephalitis in AIDS, Clin. Infect. Dis., 15:211-22). Microsporidia have been increasingly reported as pathogens in AIDS patients (Asmuth DM et al, 1994, Clinical features of microsporidosis in patients with AIDS, Clin. Infect. Dis., 18:819-25). Cryptoporidium are implicated as a cause of intractable diarrhea in AIDS (DR Arora and B Arora, Medical Parasitology, 2nd Edition, CBS Publishers and Distributors, p17). Various types of malignancies, including Hodgkin’s lymphomas, leukemias and solid tumors are associated with T gondii infection. When L. mexicana complex is inoculated into the skin of hamsters or mice, large histiocytoma tumors containing abundant amastigotes appear without inducing significant host cellular reactions (DR Arora and B Arora, Medical Parasitology, 2nd Edition, CBS Publishers and Distributors, p53: Bates PA, 1993, Axonic culture of Leishmania amastigotes, Parasitology Today, 9:143-6) which clearly show immune suppression. Such immune suppression may be achieved by protozoa through molecular mimicry. Leishmania major promastigotes were found to avoid activation of mouse bone marrow-derived macrophages (BMM0) in vitro for production of cytokines that are typically induced during infection with other intracellular pathogens (L Carrera et al, Leishmania promastigotes selectively inhibit interleukin 12 induction in bone marrow-derived macrophages from susceptible and resistant mice, J Exp Med (1996) 183: 515-26). Activation avoidance of macrophages and mechanisms that prevent an antibody response are tricky issues in diagnosis, detection and treatment.

Figuratively, the strategy of capsular molecular mimicry provides the pathogen with invisibility to the immune system. Host defense against parasites and pathogens has been recognized as a costly life-history trait that can generate trade-offs with other fitness components. However, universality of immunological costs and associated trade-offs remains questionable in animal-parasite systems (Gregory J Sandland, Dennis J Minchella, Cost of immune defense: an enigma wrapped in environmental cloak,  Trends Parasitol. 2003 Dec ;19 (12):571-4  14642767  Cit:26 ). Loss of immune defense or its compromise or impairment is a costly tragedy that is related to microparasite infections, excess free radicals from drug therapy and chemical exposure in as much as it relates to nutrition and natural antioxidant intake and must figure in the minds of the national budget planners. It is no longer a simple issue in personal health.
One of the most interesting finding by researchers is that the T. gondii protein cyclophilin 18 (C18) binds the chemokine receptor CCR5 and mediates TLR/MyD88-independent IL-12 production (Aliberti, J. et al. (2003) Nat. Immunol. 4:485) which means protozoa can hijack the interleukin system to target other invading pathogens (or cause inflammations at localized or specific sites), while competing for nutrients in the host. There is certainly a clear and obvious case of protozoal-induced AIDS or P-AIDS.  nterleukin 12 (IL-12) is an interleukin that is naturally produced by dendritic cells (Kalioski P, Hilkens CM, Snijders A, Snijdewint FG, Kapsenberg ML, 1997, "IL-12-deficient dendritic cells, generated in the presence of prostaglandin E2, promote type 2 cytokine production in maturing Human naive T helper cells," J. Immunol., 159 (1): 28–35), macrophages and human Blymphoblastoid cells (NC-37) in response to antigenic stimulation. IL-12 is involved in the differentiation of naive T cells into Th0 cells, which will further develop into either Th1 cells or Th2 cells. It is known as a T cell-stimulating factor, which can stimulate the growth and function of T cells. It stimulates the production of interferon-gamma (IFN-γ) and tumor necrosis factoralpha (TNF-α) from T and natural killer (NK) cells. IL-12 plays an important role in the activities of natural killer cells and T lymphocytes. IL-12 mediates enhancement of the immune response through the CD8+ cytotoxic T lymphocytes and the cytotoxic activity of NK cells and by priming them to target against specific pathogens (see: Kathy S. Wang, David A. Frank, and Jerome Ritz. Blood, Vol 95 No. 10 pp. 3183:3190 "Interleukin-2 enhances the response of natural killer cells to interleukin-12 through up-regulation of the interleukin-12 receptor and STAT4"). So, it is apparent that protozoa have an amazing piece of biochemistry that works on molecular mimicry for “monopolistic control” in the host to a great extent by preventing maturation and priming or avoid activation of macrophages to serve their survival. This a particular form of immune suppression.

Immune suppression involving microparasites or associated with it, may therefore be found in patients with other inflammatory disease conditions including atherosclerosis or atherosclerotic plaques as the microparasites secrete allergens that are inflammatory in nature and they can produce interleukins at the sites of infection and act through molecular mimicry.
It has not been shown, how the HIV escapes from protective immunity or immune response targeting the HIV. Microparasites and bacteria are known to have the strategy of molecular-mimicry for protection from the immune system that helps in their survival. “Certain bacteria avoid antibody defenses through molecular mimicry of common host glycan structures, masquerading as “self” to avoid immune recognition. An example is the leading pathogen, group A Streptococcus (GAS), which expresses a nonimmunogenic capsule of hyaluronan, identical to the nonsulfated glycosaminoglycan so abundant in host skin and cartilage” (ref: Victor Nizet and Jeffrey D Esko, 2009, Essentials of Glycobiology. 2nd edition, Chapter 15: Bacterial and Viral Infections, Cold Spring Harbor (NY), Bookshelf ID: NBK1952 PMID: 20301271) and tend to slow the healing process in the skin while causing pain in joints. Effectively binding their toxins and breaking up allergens and binding of broken-up allergenic proteins by phytomolecules is an essential process in therapy. Molecular-mimicry has not been proven or shown in the so called HIV.
One of the early hallmarks of HIV infection, prior to the profound depletion in CD4+ T cells, is the impairment of a variety of CD4+ T-cell functions including T-cell colony formation, autologous mixed lymphocyte reactions, expression of interleukin-2 (IL-2) receptors, and IL-2 production (for review, see Rosenberg and Fauci 1989a; cf : Victor Nizet and Jeffrey D Esko, 2009, Essentials of Glycobiology. 2nd edition, Chapter 39: Bacterial and Viral Infections, Cold Spring Harbor (NY), Bookshelf ID: NBK1952 PMID: 20301271). Interleukins are produced by microparasites as part of their molecular mimicry that enables them to establish in the host through impairment and depletion of a variety of CD4+ T-cells.
“Previous studies have demonstrated the absence of viral replication of Vif- mutants (HIV) in stimulated primary blood mononuclear cells (PBMC). Human immunodeficiency virus type 1 strain NDK Vif- mutants were propagated on the semipermissive CEM cell line, and the viral stock obtained was compared with the wild-type virus during a single cycle in PBMC. The Vif- virus was able to enter PBMC with the same efficiency as the wild type, as demonstrated by quantification of the strong-stop cDNA, and retrotranscription was observed for both viruses within 4 hr postinfection. Using a PCR assay with an Alu-long terminal repeat pair of primers, we detected integration for both the wild-type and Vif- viruses. Subsequently, qualitative and quantitative reverse transcription-mediated PCR techniques were used to study the steady-state level of intracellular and extracellular viral RNAs. All mRNA species were detected in PBMC infected with the wild-type virus or with the Vif- virus 36 hr postinfection. Furthermore, quantification of viral RNA released from infected cells demonstrated similar levels of virus produced after a unique cycle of replication. However, the Vif- virus obtained after one replication cycle in PBMC was unable to initiate retro-transcription in permissive target cells” (M Courcoul, C Patience, F Rey, D Blanc, A Harmache, J Sire, R Vigne, and B Spire, Peripheral blood mononuclear cells produce normal amounts of defective Vif- human immunodeficiency virus type 1 particles which are restricted for the preretrotranscription steps. J Virol. 1995 April; 69(4): 2068–2074).
Some of them say that the HIV retrovirus infects directly, while new research says that it requires gp120 for binding to receptor sites on the cell surface and others say the virus gains entry through a doorway at CCR5. They say that gp120 forms the viral coat and they also say that it is an enveloped virus which means that this coat is derived from the infected cell wall through the “budding process” and they also say that the “HIV gp120 molecules produced during viral replication bind to cytoplasmic CD4, forming intracellular gp120-CD4 complexes.” If the latter is true, then the HIV infection leads to viral replication and during this viral replication, the HIV gp120 is produced and it is secreted by the infected cell or is released when the infected cell dies, and it binds to the CCR5 chemokine receptor of uninfected cells! If the latter is true, the cell dies a cytopathic death and there will be no budding process. But this process naturally limits or stops the virus in healthy people who have a good intake of broad range natural antioxidants.

Cytokines are proteins which play an integral role in the human immune response. The functions of these proteins are diverse and include roles in normal T-cell-mediated immunity, the inflammatory response, cancer, autoimmunity, and allergy (Morimoto, C., N. L. Letvin, A. W. Boyd, M. Hagan, H. M. Brown, M. M. Kornacki, and S. F. Schlossman. 1985, The isolation and characterization of the human helper inducer T cell subset, The Journal of Immunology, Vol 134, Issue 6 3762-3769). Interleukins are produced by a wide variety of body cells. The function of the immune system depends in a large part on interleukins. Autoimmune diseases and immune deficiency conditions may feature deficiencies of a number of interleukins. The majority of interleukins are synthesized by helper CD4+ T lymphocytes, as well as through monocytes, macrophages, and endothelial cells. They promote the development and differentiation of T, B, and hematopoietic cells. Some of them participate in the regulation of the immune system. IL-1α is produced mainly by activated macrophages, as well as neutrophils, epithelial cells, and endothelial cells. In general, Interleukin 1 is responsible for the production of inflammation, as well as the promotion of fever and sepsis. The immuno-surveillance theory suggests that the immune system routinely patrols the cells of the body, and, upon recognition of a cell, or group of cells, that has become cancerous, it will attempt to destroy them. This immuno-surveillance includes abnormal cells and cells that are not recognized as “self” as well as microparasites.

The production of interleukin 2 (IL-2) gamma interferon, IL-4, tumor necrosis factor alpha (TNF-alpha ), TNF-beta , IL-5, and IL-10 in vitro by peripheral blood mononuclear cells cultured from healthy immunocompetent subjects can be stimulated by mitogens, including, concanavalin A, phytohemagglutinin, pokeweed mitogen, and Staphylococcus aureus Cowen. Various pathologic conditions will be accompanied by changes in cytokine levels (Rohit K. Katial, Doris Sachanandani, Carolyn Pinney, and Michael M. Lieberman, Cytokine Production in Cell Culture by Peripheral Blood Mononuclear Cells from immunocompetent Hosts, Clinical and Diagnostic Laboratory Immunology, January 1998, p. 78-81, Vol. 5, No. 1). In normal, non-clonal populations of CD4 T cells, the production of IL 2 and IL 4 is independently regulated in the majority of cells and appears to be stimulus dependent (Carding, S. R., West, J., Woods, A. and Bottomly, K. (1989), Differential activation of cytokine genes in normal CD4-bearing T cells is stimulus dependent. European Journal of Immunology, 19: 231–238).

Concurrent infections with multiple parasites are ubiquitous in nature. Ecology of disease is now getting more recognition especially those involving immune suppression. Co-infection with parasites and microparasites has important implication in bio-medicine as they compete for micronutrients and due to their systemic immunological effects via cytokines. They deplete vitamin B12 which is used in protein synthesis. It is known that co-infection by microparasites affects the immune system: the greater the helminth-induced suppression of the inflammatory cytokine interferon (IFN)-alpha, the greater the increase in microparasite density (Andrea L. Graham, Ecological rules governing helminth–microparasite co-infection, 566–570, PNAS January 15, 2008 _ vol. 105 _ no. 2).

“Immune regulation by parasites is a global concept that includes suppression, diversion, and conversion of the host immune response to the benefit of the pathogen. While many microparasites escape immune attack by antigenic variation or sequestration in specialized niches, helminths appear to thrive in exposed extracellular locations, such as the lymphatics, bloodstream, or gastrointestinal tract. We review here the multiple layers of immunoregulation that have now been discovered in helminth infection and discuss both the cellular and the molecular interactions involved. Key events among the host cell population are dominance of the T-helper 2 cell (Th2) phenotype and the selective loss of effector activity, against a background of regulatory T cells, alternatively activated macrophages, and Th2-inducing dendritic cells. Increasingly, there is evidence of important effects on other innate cell types, particularly mast cells and eosinophils. The sum effect of these changes to host reactivity is to create an anti-inflammatory environment, which is most favorable to parasite survival. We hypothesize therefore that parasites have evolved specific molecular strategies to induce this conducive landscape, and we review the foremost candidate immunomodulators released by helminths, including cytokine homologs, protease inhibitors, and an intriguing set of novel products implicated in immune suppression (Maizels RM, Balic A, Gomez-Escobar N, et al, Helminth parasites--masters of regulation, Immunol Rev 2004 Oct.:89-116:cf Johns Hopkins Medline Journals). Co-infection of a host by multiple parasite species has important epidemiological and clinical implications and immune suppression deserves uppermost recognition in therapeutic protocols and interventions keeping in mind that all drugs are immunotoxic and immunosuppressive to various extents.

"IL8 (an interleukin) can be an immunosuppressive cytokine, especially in people with AIDS or chronic lung infections (bacterial infections, pneumonia, tuberculosis). Glutathione is inversely correlated with IL8 in serum in both HIV-infected and non-infected persons and it (SeGSHPx) can inhibit IL8 release by endothelial cells. High levels of IL8 were found in tuberculosis patients who died in contrast to those who survived" (Baum, M.K. et al, 2000, "Selenium and interleukins in persons infected with human immunodeficiency virus type 1" J Infec. Dis., 182: s69-s73). Oxidative stress tends to deplete glutathione levels and AIDS patients are generally low in glutathione. Low glutathione levels and "diminished selenium-status and excessive NFKB activation is a major factor in moving HIV-infected people into full blown AIDS" (Baum et al, 2000, "Selenium and interleukins in persons infected with human immunodeficiency virus type 1" J Infec Dis 182: s69-s73).

An extremely meaningful study was carried out in the field of prevention of immune dysfunction. In their 1999 study, Zhang and colleagues infected female mice with a leukaemia retrovirus that induced mouse AIDS. They observed that the retrovirus infection reduced the release of TH1 cytokines but stimulated the release of TH2 cytokines which increased liver lipid peroxidation and caused a vitamin E deficiency. Natural vitamin E is also depleted by perhydroxyl radicals. Treatment with DHEA or melatonin (MLT), alone or in combination "largely prevented the reduction of B- and T-cell proliferation as well as of Th1 cytokine secretion caused by retrovirus infection. Supplementation also suppressed the elevated production of Th2 cytokines stimulated by retrovirus infection. DHEA and MLT simultaneously reduced lipid peroxidation in the liver and prevented vitamin E loss" (Zhang et al, 1999, Prevention of immune dysfunction and vitamin E loss by dehydroepiandrosterone and melatonin supplementation during retrovirus infection, Immunol 96: 291-97). Dr Gallo also got his “infective particle” from leukaemia patients which he claimed that it was a virus that selectively targets the cells of the immune system to cause AIDS. Again, as it is seen here, the immune suppression is mediated through cytokine-induced oxidative damage and can be reversed through natural antioxidants and it is expected that such results will be better if glutathione is also administered together with such natural antioxidants. So, did Dr. Gallo and his colleagues actually come across a new virus, they call the HIV or was he dealing only with particulate matter occurring at a certain band in supernatants or is it just a variant of leukemic retroviruses?

A new micro-particulate form of beta-(1--> 3)-D-glucan (MG) from Saccharomyces cerevisiae (yeast) for its ability to induce proinflammatory cytokine secretion in mouse peritoneal macrophages in vitro was found that was rapidly phagocytized by peritoneal macrophages, and these MG-treated macrophages up-regulated TNF-alpha, IL-6, and IL-1beta mRNAs and secreted these proinflammatory cytokines (IL 1 and TNF Alpha Production: Hunter KW, Jr. Berner MD, Sura ME Alvea BN, “IFN-gamma primes macrophages for enhanced TNF-alpha expression in response to stimulatory and non-stimulatory amounts of microparticulate beta-glucan.,” Immunol Lett ; 15:98(1): 115-22. Department of Microbiology and Immunology, University of Nevada School of Medicine, Applied Research Facility, MS-199, Reno, NV 89557, USA. April 2005). This research again supports the findings that immune suppression can be mediated through elevated levels of cytokines mediated by other substances or perhaps even by natural biomolecules such as actins that break-up by cleavage caused by oxidative stress which is in fact oxidative injury to molecules by excess free radicals arising from the phagocytic process that may involve the “oxidative burst” and requires natural antioxidants to help the cell to normalize again.
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 of 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.” (ref: Beldeu Singh, Dec 2006, Don’t Question the Gallo–HIV AIDS Dogma, Alberta Reappraising AIDS Society). This may be largely due to the fact that micro- particulate matter in the Gallo supernatants in itself has little or no infectivity.
AIDS does not behave 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 medications and oxidative stress factors that indirectly, impair cell junctions to allow easy entry of viruses into cells.
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 multi-factorial, brought on by several simultaneous strains on the immune system - drugs, pharmaceutical and recreational, sexually transmitted diseases, multiple viral infections,” (Spin June 1992) and oxidative stress caused by recreational drugs and anal lubricants and associated in others who suffer chemical exposures and malnutrition (see: Aids, Non-HIV Aids and Prescription Aids:
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) and manipulated by flawed initial clinical trials to market toxic drugs that can induce immune suppression and can cause the same symptoms like those in AIDS..
'HIV' is an artifact of cell-culture created by Dr Robert Gallo as a result of “little knowledge is a dangerous thing” and misinterpretation and having relied on a report that stated that the 1.16gm/ml band, in supernatants, which is used for “biochemical and serological analyses” is “considered to contain a population of relatively pure virus particles” but instead contains contaminants and micro-particulate matter. 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. (ref: Beldeu Singh, Dec 2006, Don’t Question the Gallo–HIV AIDS Dogma, Alberta Reappraising AIDS Society). And it clearly shows that supernatants cannot be used in place of properly obtained isolates. Using particulate matter from Gallo’s supernatants will not yield a true antibody against a retrovirus to create a vaccine, which many of the HIV researchers say is not a “protective antibody”, and more so, when Nancy Pandian has reported its extremely low infectivity – it’s a catch 22 situation.
If the components of "HIV" have been isolated and are unique to "HIV," why did Barre-Sinoussi (one of Luc Montagnier’s original group from whom Dr. Gallo hijacked LAV, later to be called “HIV”) come out of the closet, and say at the Toronto International AIDS festival last August that (ref: 109 Questions for Robert Gallo and other HIV/AIDS "experts":
 “It is not clear if therapeutic vaccines might be useful, since 15 trials to date have not demonstrated definitive evidence of improved outcomes.”

Years ago, based on their pseudo-science and the oxidative theory of AIDS, it was predicted that there will be no vaccine for HIV-AIDS (There Will Never Be a Vaccine for HIV-AIDS; The chimps that were freed after 30 years of experimenting prove just that.
The HIV postulate 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. This could not be reconciled 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” that can be divided into three groups:
1. Long-term non-progressors 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 the AIDS posse began to 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. However, when looked at through the production of glycol-protein fragments, it is not an aggressive pathogen and most likely be the EBV. That explains why there are many people who will not progress into having AIDS, as long as their antioxidant levels are high enough to prevent the cleavage of gp160 into gp120 and gp41. At one time they also claimed 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 was also no explanation 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. It must have a large amount of genetic material to be able to do all of those things but retroviruses like the fictitious Gallo-HIV is “gifted” with too little genetic material. (ref: Beldeu Singh, Dec 2006, Don’t Question the Gallo–HIV AIDS Dogma, Alberta Reappraising AIDS Society). We know that “the genome of HIV contains only three major genes (env, gag, and pol) that direct the formation of the basic components of the virus ((see:  Victor Nizet and Jeffrey D Esko, 2009, Essentials of Glycobiology, 2nd edition, Chapter 39: Bacterial and Viral Infections, Cold Spring Harbor (NY), Bookshelf ID: NBK1952 PMID: 20301271). Hence, the HIV infection theory keeps changing, although it may be nothing more than an ordinary retrovirus or micro-particulate matter that succeeds in binding to chemokine receptor sites (CCR5 or CXCR4) to trigger the production of cytokines that, if the cytokine level is elevated, there is depletion of T cells that coincides with sufficient oxidative stress when natural antioxidant levels in the blood are low, producing lipid peroxidation and inflammations that suppress the immune system and coincides with high levels of IgE as well which clearly indicate the role from allergens from microparasites.
From the forgoing, it is apparent that a retrovirus is not directly involved in initiating the AIDS condition but is precipitated by oxidative stress that is sufficient to yield polymer actin molecules that under oxidative damage and production of gp120 under conditions of oxidative stress and supported by allergens secreted by microparasites and immune suppression caused by microparasites including immune suppression by microparasites during the trophozoites stage when their life cycle proceeds by infecting cells of the immune system including lymphocytes, neutrophils and NK cells. The viral load is only a symptom and as such it is not predictive of the progression of AIDS except in 2-4% of people with the AIDS condition.
A Taiwan University Hospital reported that five transplant patients who mistakenly received organs from a deceased HIV-positive donor continue to test HIV-negative (The Body, International News, Taiwan University Hospital: Five Recipients of HIV-Positive Organs Test HIV-Negative, September 30, 2011) and will continue to test HIV-negative as long as their natural antioxidant intake is high. When, Luc Montagnier  stated in his paper published in 1997, that “indeed, evidence that oxidative stress induces and antioxidants inhibit HIV replication and apoptotic death, suggests the use of these molecules (antioxidants) as an anti-retroviral therapy to reduce  cell death in AIDS patients,” He was probably right in his observation on the association with oxidative stress and the progression of AIDS but that mechanism does not aid the replication of the virus but rather, it aids the free radical cleavage of retrovirus glycol-proteins (which are not specific to a particular retrovirus) like the EBV and when the cellular antioxidants are low, particularly glutathione, the cleaved glycol-proteins may activate super-antigens (SAgs) that increase pathogenicity, provided the immune system is first depressed or compromised by oxidative stress (such as due to chemical stressors, drugs, toxic medication and chronic malnutrition) and there is sufficient viral load and the threshold varies from person to person, depending on blood antioxidant levels and selenium intake. This type of situation probably did not occur in the chimps that were kept locked up in metal cages for 30 years and besides that they were probably injected with fluid from supernatants that did not contain any virus but only particulate matter that resulted in antibody response to such matter obtained from supernatants and such antibodies offer no protective value against viruses. Prolonged drug medication yields a very large number of drug-metabolites that conjugate with glutathione and are excreted as drug metabolite-glutathione conjugates leading to glutathione depletion and drug-induced immune depression followed by drug-induced immune suppression and the establishment of AIDS and opportunistic infections. In certain cases, organisms already present in the body such as P carnii, under these circumstances cannot be kept in check and disease conditions are established. 
An important issue in HIV-AIDS is its science of treatment. It is simply bizarre, tainted with a peculiar cruelty. Now, take a look at the AZT Label (see The AZT Label, Beldeu Singh). This is what the patient never sees. This label has appeared on bottles containing as little as 25 milligrams, a small fraction (1/20 to 1/50) of some patients' daily prescribed dose.


Glaxo Wellcome puts the following warning in large, bold-faced, capital letters at the start of the section in the 1998 Physician's Desk Reference that describes AZT (brand name Retrovir or Zidovudine):


"Granulocytopenia", also called "neutropenia" means that the primary cells of the immune system, neutrophils, have been depleted, along with some other cells, eosinophils and basophils, which are less numerous but still important. This condition can be mild, moderate, or severe. The clinical course of severe neutropenia, as described in the basic pathology textbook, Pathologic Basis of Disease by Robbins (5th Ed.), which is used in most medical schools to study pathology, describes what happens to people with severe neutropenia. The symptoms and signs of neutropenias are those of bacterial infections ... Robbins also states, in italics, that "the most severe forms of neutropenias are produced by drugs." In severe agranulocytosis with virtual absence of neutrophils, these infections may become so overwhelming as to cause death within a few days," (Robbins, p 631). This sounds disturbingly similar to a description of AIDS.

Only the insane would prescribe such a drug as medication for AIDS patients. In fact this is the type of chemical that is to be avoided by AIDS patients! Its use is associated with symptoms similar to that produced by HIV. Dr. Michael Lange, associate chief of infectious diseases at St. Luke's-Roosevelt Hospital in New York and one of the doctors the FDA consulted when evaluating AZT in 1987, says even he sometimes had trouble differentiating between AZT's toxic effects and AIDS itself. An article in the New England Journal of Medicine describes the muscle wasting caused by AZT and compared it to muscle wasting, called "myopathy", presumed to be caused by HIV. Their comments in the abstract are shocking: "We conclude that long-term therapy with Zidovudine can cause a toxic mitochondrial myopathy, which... is indistinguishable from the myopathy associated with primary HIV infection..." So, AZT can cause AIDS and yet 5000 scientists signed a declaration that HIV is the sole cause of AIDS. The AIDS industry is built on paradoxes and support from the mainstream media.

AZT has effects of toxicity in animals and humans. “It produces excruciating headaches; severe nausea; muscular pain; wasting of the muscles; damage to kidneys and nerves; excruciating pains in the legs; encephalitis; severe anemia requiring transfusions to stay alive; lymphoma (cancer); cancer in 49% of cases, versus 2% incidence in non AZT group; liver damage; nail dyschromia (fingernails turn black); insomnia; impotence; dementia; mania; ataxia (failure of muscular coordination); seizures; alopecia (hair falls out). It is a fairly well established fact that AZT was designed to kill the bone marrow. It causes neutropenia or leukopenia (loss of white blood cells) or bone marrow aplasia and bone marrow toxicity. White blood cells are the basis of the immune system. T cells and granulocytes, those are all parts of the immune system. You kill those with AZT and the immune system is gone,” Harvey Bialy, Research editor Bio/Technology Science Journal.

If a toxic drug like AZT can cause the symptoms of AIDS which is primarily through its free radical generating capacity, other drugs, too, will produce similar effects to different extents, depending on their toxicity and period of use and nutritional status of the individual as excess free radicals cause oxidative damage to membranes, DNA, mDNA, the cytochrome system and lowers ATP output as the antioxidant enzymes are depleted more rapidly.

APTIVUS - "Patients should be informed that APTIVUS is not a cure for HIV-1 infection and that they may continue to develop opportunistic infections and other complications associated with HIV disease. The long-term effects of APTIVUS are unknown at this time." Adverse Reactions: Neutropenia: 2.0% and Thrombocytopenia. Known side-effects – more immuno-deficiency.

ATRIPLA - "ATRIPLA is not a cure for HIV infection and patients may continue to experience illnesses associated with HIV infection, including opportunistic infections. Patients should remain under the care of a physician when using ATRIPLA."

RETROVIR – “RETROVIR is not a cure for HIV infection, and patients may continue to acquire illnesses associated with HIV infection, including opportunistic infections. Therefore, patients should be advised to seek medical care for any significant change in their health status. Retrovir (Zidovudine) has been associated with hematologic toxicity including neutropenia and severe anemia particularly in patients with advanced human immunodeficiency virus (HIV) disease.
In patients with advanced symptomatic HIV disease, anemia and neutropenia were the most significant adverse events observed. There have been reports of pancytopenia associated with the use of RETROVIR, which was reversible in most instances after discontinuance of the drug.”

VIRAMUNE - “VIRAMUNE is not a cure for HIV-1 infection; patients may continue to experience illnesses associated with advanced HIV-1 infection, including opportunistic infections. Patients should be advised to remain under the care of a physician when using VIRAMUNE. Patients developing signs or symptoms of severe skin reactions or hypersensitivity reactions (including, but not limited to, severe rash or rash accompanied by fever, general malaise, fatigue, muscle or joint aches, blisters, oral lesions, conjunctivitis, facial edema, and/or hepatitis, eosinophilia, granulocytopenia, lymphadenopathy, and renal dysfunction) must permanently discontinue VIRAMUNE and seek medical evaluation immediately.”

KALETRA – “Patients should be informed that KALETRA is not a cure for HIV infection and that they may continue to develop opportunistic infections and other complications associated with HIV disease. The long-term effects of KALETRA are unknown at this time. Hemic and Lymphatic System: Anemia, leukopenia, and lymphadenopathy. Known side effects – more immuno-deficiency.”

REYATAZ – “Patients should be informed that REYATAZ is not a cure for HIV infection and that they may continue to develop opportunistic infections and other complications associated with HIV disease. Patients should be told that there are currently no data demonstrating that therapy with REYATAZ can reduce the risk of transmitting HIV to others through sexual contact. Patients developing signs or symptoms of severe skin reactions or hypersensitivity reactions (including, but not limited to, severe rash or rash accompanied by one or more of the following: fever, general malaise, muscle or joint aches, blisters, oral lesions, conjunctivitis, facial edema, hepatitis, eosinophilia, granulocytopenia, lymphadenopathy, and renal dysfunction) must discontinue REYATAZ and seek medical evaluation immediately.”

INVIRASE – “Patients should be informed that INVIRASE is not a cure for HIV infection and that they may continue to acquire illnesses associated with advanced HIV infection, including opportunistic infections. Hematologic: anemia, bleeding dermal, haemolytic anemia, leucopenia, microhemorrhages, neutropenia, pancytopenia, splenomegaly, thrombocytopenia, thrombocytopenia leading to death. Known side-effects – more immuno-deficiency.”

ZIAGEN – “ZIAGEN is not a cure for HIV infection and patients may continue to experience illnesses associated with HIV infection, including opportunistic infections. Patients should remain under the care of a physician when using ZIAGEN. Patients should be advised that the use of ZIAGEN has not been shown to reduce the risk of transmission of HIV to others through sexual contact or blood contamination. Laboratory abnormalities include elevated liver function tests, increased creatine phosphokinase or creatinine, and lymphopenia.”

RESCRIPTOR – “Patients should be informed that RESCRIPTOR is not a cure for HIV-1 infection and that they may continue to acquire illnesses associated with HIV-1 infection, including opportunistic infections. Treatment with RESCRIPTOR has not been shown to reduce the incidence or frequency of such illnesses, and patients should be advised to remain under the care of a physician when using RESCRIPTOR. Patients should be advised that the use of RESCRIPTOR has not been shown to reduce the risk of transmission of HIV-1. Hemic and Lymphatic System: Adenopathy, bruising, eosinophilia, granulocytosis, leukopenia, pancytopenia, purpura, spleen disorder, thrombocytopenia, and prolonged prothrombin time.”

Anti-retroviral drugs (ARVs) do not work against micro-particulate matter obtained in the Gallo-supernatants. If the real culprit in the precipitation of immune suppression is soluble gp120 produced by oxidative stress, these ARVs are a waste of time and money. So, they need a fictitious virus. Even if they work against the so called “HIV”, they are toxic and produce immuno-deficiency or forms of immuno-deficiencies and fatigue. Extracts from patient information state that they are not a cure for HIV infection but their known side-effects can be rather adverse and clearly appear to work against the immune system and their prolonged use will actually destroy it (ref: Hence, it is not surprising at all when “Dr. Michael Lange, associate chief of infectious diseases at St. Luke's-Roosevelt Hospital in New York and one of the doctors the FDA consulted when evaluating AZT in 1987, says even he sometimes had trouble differentiating between AZT's toxic effects and AIDS itself.” Truth be known about the morals and philosophy of modern medicine.

No comments:

Post a Comment