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A well-rounded forum for the mental meanderings of those (mostly Paul Murray at this stage) who don't necessarily subscribe to the paradigm that we are THE most sentient beings in the universe and got here exactly as the anthropologists reckon we did... among insane humour & other controversial subject matter... PRANA: Life force energy - i.e. the stuff that enlivens us, synonymous with the soul - in Native American speak: Wakan Tanka - the Great Spirit that moves through all things..
Paul
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Half the story is a dangerous thing
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2 comments:
Factors Known to Cause False-Positive HIV Antibody Test Results
1. Anti-carbohydrate antibodies (52, 19, 13)
2. Naturally-occurring antibodies (5, 19)
3. Passive immunization: receipt of gamma globulin or immune globulin (as prophylaxis against infection which contains antibodies)(18, 26, 60, 4, 22, 42, 43, 13)
4. Leprosy (2, 25)
5. Tuberculosis (25)
6. Mycobacterium avium (25)
Systemic lupus erythematosus (15, 23)
7. Renal (kidney) failure (48, 23, 13)
8. Hemodialysis/renal failure (56, 16, 41, 10, 49)
9. Alpha interferon therapy in hemodialysis patients (54)
10. Flu (36)
11. Flu vaccination (30, 11, 3, 20, 13, 43)
12. Herpes simplex I (27)
13. Herpes simplex II (11)
14. Upper respiratory tract infection (cold or flu)(11)
15. Recent viral infection or exposure to viral vaccines (11)
16. Pregnancy in multiparous (i.e. recurrently pregnant)women (58, 53, 13, 43, 36)
17. Malaria (6, 12)
18. High levels of circulating immune complexes (6, 33)
19. Hypergammaglobulinemia (high levels of antibodies) (40, 33)
20. False positives on other tests, including RPR (rapid plasma reagent) test for syphilis (17, 48, 33, 10, 49)
21. Rheumatoid arthritis (36)
22. Hepatitis B vaccination (28, 21, 40, 43)
23. Tetanus vaccination (40)
24. Organ transplantation (1, 36)
25. Renal transplantation (35, 9, 48, 13, 56)
26. Anti-lymphocyte antibodies (56, 31)
27. Anti-collagen antibodies (found in gay men, haemophiliacs, Africans of both sexes and people with leprosy)(31)
28. Serum-positive for rheumatoid factor, antinuclear antibody (both found in rheumatoid arthritis and other autoantibodies)(14, 62, 53)
29. Autoimmune diseases (44, 29, 10, 40, 49, 43): Systemic lupus erythematosus, scleroderma, connective tissue disease, dermatomyositis
30. Acute viral infections, DNA viral infections (59, 48, 43, 53, 40, 13)
31. Malignant neoplasms (cancers)(40)
32. Alcoholic hepatitis/alcoholic liver disease (32, 48, 40,10,13, 49, 43, 53)
33. Primary sclerosing cholangitis (48, 53)
34. Hepatitis (54)
35. "Sticky" blood (in Africans) (38, 34, 40)
36. Antibodies with a high affinity for polystyrene (used in the test kits)(62, 40, 3)
37. Blood transfusions, multiple blood transfusions (63, 36,13, 49, 43, 41)
38. Multiple myeloma (10, 43, 53)
39. HLA antibodies (to Class I and II leukocyte antigens)(7, 46, 63, 48, 10, 13, 49, 43, 53)
40. Anti-smooth muscle antibody (48)
41. Anti-parietal cell antibody (48)
42. Anti-hepatitis A IgM (antibody)(48)
43. Anti-Hbc IgM (48)
44. Administration of human immunoglobulin preparations pooled before 1985 (10)
45. Haemophilia (10, 49)
46. Haematologic malignant disorders/lymphoma (43, 53, 9, 48, 13)
47. Primary biliary cirrhosis (43, 53, 13, 48)
48. Stevens-Johnson syndrome9, (48, 13)
49. Q-fever with associated hepatitis (61)
50. Heat-treated specimens (51, 57, 24, 49, 48)
51. Lipemic serum (blood with high levels of fat or lipids)(49)
52. Haemolyzed serum (blood where haemoglobin is separated from the red cells)(49)
53. Hyperbilirubinemia (10, 13)
54. Globulins produced during polyclonal gammopathies (which are seen in AIDS risk groups)(10, 13, 48)
55. Healthy individuals as a result of poorly-understood cross-reactions (10)
56. Normal human ribonucleoproteins (48,13)
57. Other retroviruses (8, 55, 14, 48, 13)
58. Anti-mitochondrial antibodies (48, 13)
59. Anti-nuclear antibodies (48, 13, 53)
60. Anti-microsomal antibodies (34)
61. T-cell leukocyte antigen antibodies (48, 13)
62. Proteins on the filter paper (13)
63. Epstein-Barr virus (37)
64. Visceral leishmaniasis (45)
65. Receptive anal sex (39, 64)
References
1. Agbalika F, Ferchal F, Garnier J-P, et al. 1992. False-positive antigens related to emergence of a 25-30 kD protein detected in organ recipients. AIDS. 6:959-962.
2. Andrade V, Avelleira JC, Marques A, et al. 1991. Leprosy as a cause of false-positive results in serological assays for the detection of antibodies to HIV-1. Intl. J. Leprosy. 59:125.
3. Arnold NL, Slade RA, Jones MM, et al. 1994. Donor follow up of influenza vaccine-related multiple viral enzyme immunoassay reactivity. Vox Sanguinis. 67:191.
4. Ascher D, Roberts C. 1993. Determination of the etiology of seroreversals in HIV testing by antibody fingerprinting. AIDS. 6:241.
5. Barbacid M, Bolgnesi D, Aaronson S. 1980. Humans have antibodies capable of recognizing oncoviral glycoproteins: Demonstration that these antibodies are formed in response to cellular modification of glycoproteins rather than as consequence of exposure to virus. Proc. Natl. Acad. Sci. 77:1617-1621.
6. Biggar R, Melbye M, Sarin P, et al. 1985. ELISA HTLV retrovirus antibody reactivity associated with malaria and immune complexes in healthy Africans. Lancet. ii:520-543.
7. Blanton M, Balakrishnan K, Dumaswala U, et al. 1987. HLA antibodies in blood donors with reactive screening tests for antibody to the immunodeficiency virus. Transfusion. 27(1):118.
8. Blomberg J, Vincic E, Jonsson C, et al. 1990. Identification of regions of HIV-1 p24 reactive with sera which give "indeterminate" results in electrophoretic immunoblots with the help of long synthetic peptides. AIDS Res. Hum. Retro. 6:1363.
9. Burkhardt U, Mertens T, Eggers H. 1987. Comparison of two commercially available anti-HIV ELISA's: Abbott HTLV-III ELA and DuPont HTLV-III ELISA. J. Med. Vir. 23:217.
10. Bylund D, Ziegner U, Hooper D. 1992 Review of testing for human immunodeficiency virus. Clin. Lab. Med. 12:305-333.
11. Challakere K, Rapaport M. 1993. False-positive human immunodeficiency virus type 1 ELISA results in low-risk subjects. West. J. Med. 159(2):214-215.
12. Charmot G, Simon F. 1990. HIV infection and malaria. Revue du practicien. 40:2141.
13. Cordes R, Ryan M. 1995. Pitfalls in HIV testing. Postgraduate Medicine. 98:177.
14. Dock N, Lamberson H, O'Brien T, et al. 1988. Evaluation of atypical human immunodeficiency virus immunoblot reactivity in blood donors. Transfusion. 28:142.
15. Esteva M, Blasini A, Ogly D, et al. 1992. False positive results for antibody to HIV in two men with systemic lupus erythematosus. Ann. Rheum. Dis. 51:1071-1073.
16. Fassbinder W, Kuhni P, Neumayer H. et al. 1986. Prevalence of antibodies against LAV/HTLV-III [HIV] in patients with terminal renal insufficiency treated with hemodialysis and following renal transplantation. Deutsche Medizinische Wochenschrift. 111:1087.
17. Fleming D, Cochi S, Steece R. et al. 1987. Acquired immunodeficiency syndrome in low-incidence areas. JAMA. 258(6):785.
18. Gill MJ, Rachlis A, Anand C. 1991. Five cases of erroneously diagnosed HIV infection. Can. Med. Asso. J. 145(12):1593.
19. Healey D, Bolton W. 1993. Apparent HIV-1 glycoprotein reactivity on Western blot in uninfected blood donors. AIDS. 7:655-658.
20. Hisa J. 1993. False-positive ELISA for human immunodeficiency virus after influenza vaccination. JID. 167:989.
21. Isaacman S. 1989. Positive HIV antibody test results after treatment with hepatitis B immune globulin. JAMA. 262:209.
22. Jackson G, Rubenis M, Knigge M, et al. 1988. Passive immunoneutralisation of human immunodeficiency virus in patients with advanced AIDS. Lancet, Sept. 17:647.
23. Jindal R, Solomon M, Burrows L. 1993. False positive tests for HIV in a woman with lupus and renal failure. NEJM. 328:1281-1282.
24. Jungkind D, DiRenzo S, Young S. 1986. Effect of using heat-inactivated serum with the Abbott human T-cell lymphotropic virus type III [HIV] antibody test. J. Clin. Micro. 23:381.
25. Kashala O, Marlink R, Ilunga M. et al. 1994. Infection with human immunodeficiency virus type 1 (HIV-1) and human T-cell lymphotropic viruses among leprosy patients and contacts: correlation between HIV-1 cross-reactivity and antibodies to lipoarabionomanna. J. Infect. Dis. 169:296-304.
26. Lai-Goldman M, McBride J, Howanitz P, et al. 1987. Presence of HTLV-III [HIV] antibodies in immune serum globulin preparations. Am. J. Clin. Path. 87:635.
27. Langedijk J, Vos W, Doornum G, et al. 1992. Identification of cross-reactive epitopes recognized by HIV-1 false-positive sera. AIDS. 6:1547-1548.
28. Lee D, Eby W, Molinaro G. 1992. HIV false positivity after hepatitis B vaccination. Lancet. 339:1060.
29. Leo-Amador G, Ramirez-Rodriguez J, Galvan-Villegas F, et al. 1990. Antibodies against human immunodeficiency virus in generalized lupus erythematosus. Salud Publica de Mexico. 32:15.
30. Mackenzie W, Davis J, Peterson D. et al. 1992. Multiple false-positive serologic tests for HIV, HTLV-1 and hepatitis C following influenza vaccination, 1991. JAMA. 268:1015-1017.
31. Mathe G. 1992. Is the AIDS virus responsible for the disease? Biomed & Pharmacother. 46:1-2.
32. Mendenhall C, Roselle G, Grossman C, et al. 1986. False-positive tests for HTLV-III [HIV] antibodies in alcoholic patients with hepatitis. NEJM. 314:921.
33. Moore J, Cone E, Alexander S. 1986. HTLV-III [HIV] seropositivity in 1971-1972 parenteral drug abusers - a case of false-positives or evidence of viral exposure? NEJM. 314:1387-1388.
34. Mortimer P, Mortimer J, Parry J. 1985. Which anti-HTLV-III/LAV [HIV] assays for screening and comfirmatory testing? Lancet. Oct. 19, p873.
35. Neale T, Dagger J, Fong R, et al. 1985. False-positive anti-HTLV-III [HIV] serology. New Zealand Med. J. October 23.
36. Ng V. 1991. Serological diagnosis with recombinant peptides/proteins. Clin. Chem. 37:1667-1668.
37. Ozanne G, Fauvel M. 1988. Perfomance and reliability of five commercial enzyme-linked immunosorbent assay kits in screening for anti-human immunodeficiency virus antibody in high-risk subjects. J. Clin. Micro. 26:1496.
38. Papadopulos-Eleopulos E. 1988. Reappraisal of AIDS - Is the oxidation induced by the risk factors the primary cause? Med. Hypo. 25:151.
39. Papadopulos-Eleopulos E, Turner V, and Papadimitriou J. 1993. Is a positive Western blot proof of HIV infection? Bio/Technology. June 11:696-707.
40. Pearlman ES, Ballas SK. 1994. False-positive human immunodeficiency virus screening test related to rabies vaccination. Arch. Pathol. Lab. Med. 118-805.
41. Peternan T, Lang G, Mikos N, et al. Hemodialysis/renal failure. 1986. JAMA. 255:2324.
42. Piszkewicz D. 1987. HTLV-III [HIV] antibodies after immune globulin. JAMA. 257:316.
43. Profitt MR, Yen-Lieberman B. 1993. Laboratory diagnosis of human immunodeficiency virus infection. Inf. Dis. Clin. North Am. 7:203.
44. Ranki A, Kurki P, Reipponen S, et al. 1992. Antibodies to retroviral proteins in autoimmune connective tissue disease. Arthritis and Rheumatism. 35:1483.
45. Ribeiro T, Brites C, Moreira E, et al. 1993. Serologic validation of HIV infection in a tropical area. JAIDS. 6:319.
46. Sayers M, Beatty P, Hansen J. 1986. HLA antibodies as a cause of false-positive reactions in screening enzyme immunoassays for antibodies to human T-lymphotropic virus type III [HIV]. Transfusion. 26(1):114.
47. Sayre KR, Dodd RY, Tegtmeier G, et al. 1996. False-positive human immunodeficiency virus type 1 Western blot tests in non-infected blood donors. Transfusion. 36:45.
48. Schleupner CJ. Detection of HIV-1 infection. In: (Mandell GI, Douglas RG, Bennett JE, eds.) Principles and Practice of Infectious Diseases, 3rd ed. New York: Churchill Livingstone, 1990:1092.
49. Schochetman G, George J. 1992. Serologic tests for the detection of human immunodeficiency virus infection. In AIDS Testing Methodology and Management Issues, Springer-Verlag, New York.
50. Simonsen L, Buffington J, Shapiro C, et al. 1995. Multiple false reactions in viral antibody screening assays after influenza vaccination. Am. J. Epidem. 141-1089.
51. Smith D, Dewhurst S, Shepherd S, et al. 1987. False-positive enzyme-linked immunosorbent assay reactions for antibody to human immunodeficiency virus in a population of midwestern patients with congenital bleeding disorders. Transfusion. 127:112.
52. Snyder H, Fleissner E. 1980. Specificity of human antibodies to oncovirus glycoproteins; Recognition of antigen by natural antibodies directed against carbohydrate structures. Proc. Natl. Acad. Sci. 77:1622-1626.
53. Steckelberg JM, Cockerill F. 1988. Serologic testing for human immunodeficiency virus antibodies. Mayo Clin. Proc. 63:373.
54. Sungar C, Akpolat T, Ozkuyumcu C, et al. Alpha interferon therapy in hemodialysis patients. Nephron. 67:251.
55. Tribe D, Reed D, Lindell P, et al. 1988. Antibodies reactive with human immunodeficiency virus gag-coated antigens (gag reactive only) are a major cause of enzyme-linked immunosorbent assay reactivity in a bood donor population. J. Clin. Micro. April:641.
56. Ujhelyi E, Fust G, Illei G, et al. 1989. Different types of false positive anti-HIV reactions in patients on hemodialysis. Immun. Let. 22:35-40.
57. Van Beers D, Duys M, Maes M, et al. Heat inactivation of serum may interfere with tests for antibodies to LAV/HTLV-III [HIV]. J. Vir. Meth. 12:329.
58. Voevodin A. 1992. HIV screening in Russia. Lancet. 339:1548.
59. Weber B, Moshtaghi-Borojeni M, Brunner M, et al. 1995. Evaluation of the reliability of six current anti-HIV-1/HIV-2 enzyme immunoassays. J. Vir. Meth. 55:97.
60. Wood C, Williams A, McNamara J, et al. 1986. Antibody against the human immunodeficiency virus in commercial intravenous gammaglobulin preparations. Ann. Int. Med. 105:536.
61. Yale S, Degroen P, Tooson J, et al. 1994. Unusual aspects of acute Q fever-associated hepatitis. Mayo Clin. Proc. 69:769.
62. Yoshida T, Matsui T, Kobayashi M, et al. 1987. Evaluation of passive particle agglutination test for antibody to human immunodeficiency virus. J. Clin. Micro. Aug:1433.
63. Yu S, Fong C, Landry M, et al. 1989. A false positive HIV antibody reaction due to transfusion-induced HLA-DR4 sensitization. NEJM.320:1495.
64. National Institue of Justice, AIDS Bulletin. Oct. 1988.
Top 100 AIDS Science Inconsistencies
All of the observations below can be substantiated by independent research. How long can the HIV=AIDS=Death dogma be maintained in the face of so many scientific cracks?
1. AIDS occurs in the absence of HIV (65, 87), a new medical definition (Idiopathic CD4+ T-cell lymphocytopenia) was therefore created.
2. HIV does not satisfy Koch’s postulates, the criteria that must be met in order to prove that a microbe causes a disease (90)
3. Anti-HIV drugs, including protease inhibitors, destroy T-cells (4-10)
4. Septrin (also called Septra, Bactrim, Co-trimoxazole) and anti-HIV drugs destroy mitochondria (11,12)
5. The PCP (Pneumocystis Carinii pneumonia) fungus becomes resistant to Septrin (12)
6. Recreational drugs (heroin, poppers, crystal met, ecstasy, cocaine) reduce CD4 cell numbers (13-18, 58, 66-68)
7. HIV positive patients recover after they stop taking drugs (58)
8. Recreational drugs cause AIDS-defining diseases (see table 7 of 58)
9. Anti-HIV drugs cause AIDS-defining diseases (58)
10. Anti-HIV drugs inhibit human enzymes (11)
11. HIV positive Africans in dire poverty in Uganda and no access to anti-HIV drugs lived as long as HIV positives in the West who took anti-HIV drugs (33)
12. There are no comparative studies of survival in HIV negatives and combo-free HIV positive heterosexuals with no other risk factors.
13. Only 38% of healthy long-term positives had ever used AZT or other nucleoside analogs compared with 94% of progressors (80)
14. Decreases in AIDS cases preceded the introduction of new drug treatments (Dec 1995) by three full years (see fig. 6 of 106)
15. Anti-HIV drugs have anti-microbial effects (49, 50, 10)
16. The introduction of AZT did not cause a decline in the AIDS death rate (105)
17. In the only long term trial of AZT (The Concorde study) 172 participants died, 169 while taking AZT, 3 while on placebo (51)
18. Nucleoside analog drugs suppress/destroy the bone marrow where all immune system cells are born (26, 32, 111)
19. HIV+ children born to AZT treated mothers had a higher probability of developing severe disease or severe immunosuppression (53)
20. “Drug holidays” recover immune responses
21. AZT caused the same transient increase in CD4 count in HIV negatives as in HIV positives (55)
22. There are no controlled studies showing that AIDS occurs in the absense of all other possible non-HIV causal factors.
23. Long-living, healthy, drug-free HIV positives are mostly ignored by AIDS researchers
24. Apart from the early (fraudulent) AZT studies and the Concorde study no efficacy studies compare drugs with placebo
25. There are well documented, non-HIV causes for every AIDS disease
26. The incidence of AIDS-defining diseases among Western non-drug users has not been shown to exceed national backgrounds (58)
27. Early AIDS coincided with the cumulative effects of unprecedented, intense use of volatile nitrite (poppers) as a aphrodisiac marketed almost exclusively to homosexuals (102)
28. AIDS can be treated effectively without anti-HIV drugs (39-42, 112)
29. On average viral load overestimates infectious HIV by a factor of 60,000 (21)
30. Even a PCR method that can detect 1 infected cell in 100000 found very little HIV DNA in HIV positives (23)
31. HIV could not be cultured from people with a detectable viral load (19, 21)
32. HIV has never been properly isolated (20)
33. After many billions of dollars of research effort over 20 years, HIV scientists still cannot explain how HIV causes AIDS.
34. After many billions of dollars of research effort over 20 years there is no vaccine and no cure, there are only toxic drugs
35. There was no increase in HIV seroprevalence outside risk groups in the UK despite record STD rates and teenage pregnancy rates (25)
36. HIV DNA was found to be constant from the time of seroconversion but CD4 count continually went down (29)
37. CD4 count goes down and viral load goes up while on the anti-HIV drugs.
38. AZT is hardly triphosphorylated by the body so it cannot possibly have an anti-HIV effect (30)
39. AZT has no effect on HIV DNA but makes viral load (HIV RNA) go down (31)
40. Research throughout the 1970s showed that retroviruses do not kill cells.
41. The probability of heterosexual transmission of HIV was found to be very low (1 in a 1000 for male to female and 8 times less likely for female to male) (34)
42. HIV antibody tests can give repeated false positives and seroreversions can occur (95-100, 114-116)
43. HIV tests are sensitive to non-specific antibody binding
44. HIV tests involve an arbitrary dilution factor, everyone tests positive (because of non-specific antibody binding) if their serum is undiluted (104)
45. All the proteins used in the HIV test are associated with retroviral genes that are found naturally (endogenous) in all humans (72)
46. Endogenous retroviruses can generate immune responses in humans (73, 74)
47. None of the HIV proteins tested for have been proven to belong to HIV (75)
48. There are over 60 different conditions, including pregnancy, that have been known to generate false positives on the HIV test (91)
49. The Elisa, Western Blot and PCR tests for HIV all carry disclaimers nullifying their detection of HIV
50. The criteria for HIV-positivity used in the antibody tests varies between countries and between organisations within a country and can produce indeterminate (neither positive or negative) results (75, 109) The Western Blot HIV test, widely regarded as the most accurate, is not used in England and Wales because it is regarded as inaccurate.
51. The viral load PCR primers were found to be non-specific for “HIV” genetic sequences (35)
52. The viral load test gives false negatives (36)
53. The viral load test gives false positives (36, 113)
54. The viral load test has low reproducibility (36-38)
55. Direct measurements showed no correlation between viral load and CD4 count (43)
56. Many conditions cause reduced CD4 counts (86)
57. CD4 counts between 200 and 300 have been observed in healthy HIV negatives (87)
58. There are no studies comparing CD4 cell variations in combo-free HIV positives (with no risk factors) and HIV negatives.
59. According to the AIDS establishment, a heterosexual AIDS “epidemic” of African origin started off in the West as a homosexual “epidemic”
60. In 1985 HIV incidence in Southern Africa was confined to homosexuals who had been to the US and those who had had sex with them (88, 89).
61. The USA was found to be the world’s most sexually promiscuous nation (27)
62. Condoms (made from polyisoprene) have holes in much larger than HIV (28, 110)
63. Reducing STD incidence in Africa did not reduce the rate of HIV seroconversion* (101)
64. Only a minute proportion of Africans have actually been tested for HIV, seroprevalence estimates are derived from extrapolations based on unrepresentative samples from maternity clinics.
65. In Africa a single positive ELISA test or even a single “rapid” (saliva/urine) test is considered proof of HIV infection, “proof” in the developed world requires a series of tests
66. HIV seroprevalence was found to be much lower in South African prisons than in the general population (1)
67. The vast majority of African “AIDS patients” tested HIV negative (44, 45)
68. In “AIDS ravaged” Zambia since 1980 the population has increased and even the rate of increase in population has increased! (46)
69. In “AIDS ravaged” South Africa many coffin makers are either doing a slack trade or have gone out of business (47)
70. The total number of AIDS cases in Africa consists almost entirely of estimated cases rather than known, registered cases (54)
71. PCP is the typical AIDS defining disease in Western adults but it is almost entirely confined to young children in Africa (2,3)
72. There is no Western heterosexual AIDS epidemic
73. IVDUs who consistently used a clean needle exchange program were 10.2 to 22.9 times MORE likely to test HIV positive than non-users (48)
74. Non-human primates “progress” to AIDS (SAIDS) much quicker than humans do (107)
75. SIV does not cause SAIDS in wild primate populations (108)
76. SIV seroprevalence is too low in wild primate populations to account for SIV resistance in these populations (22)
77. SIV seroprevalence in captive SIV naïve primate populations was found to be very low (22)
78. Until the early 1930s many thousands of European men received transplants from chimpanzees and did not get AIDS (62)
79. Uganda study showed HIV-positivity did not indicate a new cause of disease, only decreased mortality in HIV negatives (52)
80. One thousand medical staff a year accidentally contract hepatitis from needles yet by 1998 there were no documented cases of surgeons or emergency medical technicians/paramedics getting AIDS, or even HIV, from occupational exposure (58, Table 16 of 106)
81. All AIDS patients have lowered levels of glutathione, the major water soluble intracellular antioxidant (59, 60)
82. The antioxidant N-acetyl cysteine inhibits “HIV replication” (61)
83. Reactive oxygen species are implicated in the induction of HIV expression and cell death (40)
84. Treatment with oxidising, mitogenic*** agents is necessary for HIV “isolation” from cell culture (56, 57)
85. Significant HIV replication was found to follow rather than precede AIDS defining disease (94)
86. Low T-cell counts were shown to occur before HIV seroconversion and to predict seroconversion (92, 93)
87. HIV-like genetic sequences have been found in the HIV negative human genome (63)
88. Epitopes** of HIV regulatory proteins tat, rev and nef are expressed in normal human tissue (71, 116)
89. Toxic intracellular stresses can create novel genetic sequences (64)
90. Within a subgroup, HIV showed over 40% variation in an essential gene (protease) sequence (103)
91. Foreign protein transfusions were found to be immune suppressive (79, 81, 84, 85)
92. Haemophiliacs can have hypergammaglobulinaemia which can cause false HIV positive test results (69)
93. Up to 99.9% of HIV genomes in plasma may be defective (70)
94. Mortality in haemophiliacs began to increase in exactly the same year they began taking AZT (81, 82)
95. The AIDS risk of hemophiliacs on AZT was 4.5 times higher, and mortality 2.4 times higher, than untreated controls (83)
96. Infectious HIV (a delicate virus) does not survive the Factor VIII preparation process (76-78)
97. HIV theorists have made incorrect predictions throughout the HIV era.
98. Corticosteroids and endogenous cortisol suppress cellular immune responses and cortisol destroys immature T-cells (24)
99. Effective cellular immunity relies upon nitric oxide gas defence; see for example Eur. J. Immunol. 2002, 32(5):1455-63
100. AIDS spreads non-exponentially, unlike infectious disease (58)
5 QUESTIONS TO EXPOSE AN HIV DOCTOR
1. Why does the antibody level of HIV positives continue to rise?
2. Why does AZT cause a CD4 count increase in HIV negatives as well as in HIV positives? (1)
3. Two repeat positive ELISAs are regarded as diagnostic in England and Wales while in the rest of the Western world the Western Blot test (widely regarded as the most accurate) must be used as an additional confirmatory test. Why is this?
4. Why do direct measurements of changes in CD4 cell numbers show no correlation with viral load? (2)
5. What is the mechanism by which HIV causes AIDS?
Notes
1. According to the establishment, HIV causes AIDS by reducing the number of CD4 cells. This cannot happen because type 2 CD4 cells are responsible for stimulating antibody production. If these cells were really reduced by HIV, the antibody level of HIV positives would not continue to rise.
2. If the rise in CD4 count were really due to an anti- HIV effect of the drugs this would not happen. In reality the increase is due to type 2 CD4 cells entering the bloodstream from the bone marrow in response to the bone marrow toxicity of the drug.
3. HIV positivity is an arbitrary rather than an absolute definition
4. Again, if HIV causes AIDS via its effect on CD4 cells there should be a correlation.
5. The correct answer is: “No-one knows” This is because HIV does not cause AIDS
References
(1) http://bmj.com/cgi/content/full/324/7331/237 (2) American J of Respiratory and Critical Care Medicine 1994, 149(6):1591-1596
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