- Why Dr. Gallo uses supernatants and not isolates?
- 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?
- Why there are a large number of false positives with tests using these test kits, including people recovering from malaria and flu?
- Why do the HIV test kits test for p24, the significance of which is not known?
- What is the real role of gp120 in the infection process and in immune-suppression?
- 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”?
- What is the treatment for drug-induced AIDS? More of the toxic medication?
- If AIDS is caused by a virus, why is there a latency period?
- "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).
- 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).
- 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.
- 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.
- Fewer, or no, copy numbers of pathogen-associated nucleic acid sequences should occur in hosts or tissues without disease.
- 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.
- 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.
- The nature of the microorganism inferred from the available sequence should be consistent with the known biological characteristics of that group of organisms.
- 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.
- These sequence-based forms of evidence for microbial causation should be reproducible.
“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.
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.
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-), TNF-, 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).
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.”