Re THINKING HIV AIDS

Sabtu, 09 Februari 2013

NANCY TURNER BANKS - THE DEADLY FALSE HIV VIRUS OF INTERNATIONAL GREED

October 6th, 2010
This Harvard-trained MD who also has an MBA has recently published her book “AIDS, Opium, Diamonds and Empire”, subtitled “The Deadly Virus of International Greed. Nancy had a wide ranging discussion with Terry Michael and David Crowe for almost an hour.Nancy’s excellent book can be purchased from Amazon, The Book Depository (UK) or the publisher iUniverse. Dr. Banks also maintains a website on medicine and politics at nancybanks.us.
http://www.howpositiveareyou.com/
Remember a long time before ‘House of Numbers’ we had ‘HIV – Fact or Fiction?’ and ‘The Other Side of AIDS’. These two films are the real gems.

Selasa, 29 Januari 2013

Pemusnahan ETNIS melalui VIRUS

Program Rahasia Virus Amerika

Posted: November 29, 2012 by dodyaero in Artikel

Orang kulit hitam memiliki gen yang disebut CCR5 delta 32 + (termasuk orang berkulit coklat) Di ujung lain dari spektrum adalah CCR5 delta 32 -. CCR5 Delta 32 – adalah mutasi CCR5 delta 32 + yang asli. Satu-satunya orang yang memiliki gen Delta 32- adalah orang-orang kulit Putih – Bangsa Eropa Nordik.

Sebanyak 32 alel harus diwariskan dari kedua orang tuanya untuk menjadi kebal terhadap tes HIV dan AIDS. Gen yang bermutasi ini tidak memiliki wadah yang diperlukan untuk “mempertahankan” HIV dan Penyakit AIDS. Gen memberikan kepercayaan terhadap penyakit yang rasial dan dirancang untuk menghilangkan “orang kulit berwarna.” Sekitar 10 persen orang Eropa membawa gen mutasi Delta CCR5 32 -. Kejadian ini hanya 2 persen di Asia Tengah, dan mutasi sama sekali tidak ada di antara orang Asia Timur, Afrika, dan Indian Amerika. DAN INI SEMESTINYA MEMBERIKAN ANDA SEBUAH INFORMASI.

Enzim HIV / AIDS adalah produk dari banyak langkah di laboratorium yang sesuai dengan segala kriteria ilmiah dalam setiap kajian independen ‘de novo’ yang telah dilakukan sampai saat ini. Sejarah ilmu pengetahuan menunjukkan sebuah ‘obsesi Arya’ dengan pengembangan senjata biologis etnis menargetkan orang-orang keturunan bersifat Negro. Saat ini tidak jelas kapan tepatnya “genociders” (pelaku genosida) mempelajari ada perbedaan yang dieksploitasi dalam darah ras Negro.

Tak lama setelah Kongres Amerika Serikat memberikan anggaran dana (untuk senjata biologis ofensif) kepada CIA dan militer AS pada tahun 1957, anak-anak Negro di Benua Afrika menjadi menderita kanker “jenis baru” (Limfoma Burkitt). Pada tahun 2002 sesuatu atau beberapa penyakit baru sedang membunuh anak-anak Afrika yang memanfaatkan gen CCR5 delta 32+ — yang terdapat pada semua orang kulit berwarna. Ini menjadi jelas ada master plan yang jelas untuk melemahkan, melumpuhkan, memberantas dan menghilangkan populasi kulit hitam di dunia.

Perpustakaan Kedokteran Nasional menentukan frekuensi dari alel mutan CCR5 delta 32 pada populasi berisiko tinggi HIV-yang seronegatif, dan menemukan keberhasilan perlindungan in vitro tehadap infeksi HIV-1 jika dibandingkan dengan penduduk umum Afrika. Dalam bentuk homozigot, alel CCR5 delta 32- memberikan resistensi terhadap makrofag-tropik (M-tropik) jenis HIV-1. Dengan asumsi bahwa karakteristik genetik mendukung perlawanan HIV akan berlaku pada populasi berisiko tinggi HIV-negatif, mereka memeriksa genotipe CCR5 wanita pekerja seks komersial (PSK) dari Dakar, Senegal, yang tetap tidak terinfeksi pada jangka lama.

Metode yang digunakan adalah sebagai berikut: Profil gen CCR5 peserta penelitian ditentukan dengan polymerase chain reaction (PCR) amplifikasi dan diikuti DNA genom secara berurutan. Sel mononuklear darah perifer (PBMC) terinfeksi dengan jenis yang berbeda dari HIV-1 dan dipantau dengan menggunakan p24 enzyme-linked immunosorbent assay (ELISA).

Hasil : Mereka mengkonfirmasikan adanya dua genotipe CCR5wt/delta 32 diantara 139 orang (1,44%). PBMC dari ini 2 individu yang heterozigot juga ditemukan kurang rentan terhadap infeksi in vitro dengan sebuah M-tropik HIV-1 yang mengisolasi secara primer. Berikut ini adalah kesimpulannya: Bukti ditemukan suatu peningkatan prevalensi genotipe CCR5wt/delta 32dalam kelompok berisiko tinggi HIV-negatif di Afrika Barat. Selain itu, terjadi pengurangan kerentanan terhadap infeksi HIV-1 pada individu-individu heterozigot yang mendukung peran 32-bp CCR5 pada perlawanan penghapusan HIV-1.

Komentar dari Komunitas Nasionalis Stormfront White

Pada pertengahan tahun 1990, sebuah contoh baru yang menarik dari seleksi intens terhadap salah satu sifat homozigot yang terungkap. Ini berasal dari penemuan bahwa beberapa orang yang tidak terkena AIDS bahkan jika mereka berulang kali terkena virus (HIV) dan semestinya berakibat fatal. Orang-orang yang kebal telah mewarisi dua salinan gen mutan langka yang dikenal sebagai CCR5 delta 32 – mereka memiliki gen yang homozigot. Sedangkan mereka yang heterozigot tampaknya memiliki imunitas parsial atau setidaknya penundaan dalam timbulnya AIDS.

Sekitar 10% orang Eropa sekarang memiliki varian gen CCR5 delta 32, tetapi hal ini sangat jarang atau tidak ada pada populasi lain dunia. Ada hubungan yang mengejutkan dalam cerita ini. Gen CCR5 delta 32 juga memberikan kekebalan terhadap penyakit mematikan yang ditimbulkan oleh bakteri, wabah pes. Orang yang homozigot untuk varian gen OCR5-delta 32 benar-benar kebal, sementara yang heterozigot memiliki kekebalan parsial. Hal ini sangat mungkin bahwa alel ini yang menyelamatkan jiwa sebagai mutasi acak dan bahwa ia dipilih oleh epidemi wabah yang menghancurkan ras kulit hitam yang menyapu seluruh Eropa dimulai pada abad ke-14. Selama gelombang wabah pertama, antara 1347 dan 1350, seperempat sampai sepertiga dari semua orang Eropa meninggal karena penyakit ini. Seleksi alam menguntungkan pada mereka yang secara kebetulan mewarisi varian gen CCR5 delta 32. Gelombang wabah berulang selama tiga abad berikutnya dan mengakibatkan peningkatan frekuensi CCR5 delta 32 pada populasi Eropa.

Bukti AIDS Dikembangkan

Hukum Publik Amerika Serikat (91-213) yang ditandatangani pada 16 Maret 1970, oleh Richard Nixon menyatakan: “Dalam ‘upaya’ Amerika Serikat menstabilkan penduduk Sub-Sahara Afrika dan dengan demikian, meningkatkan keamanan nasional masa depan Amerika Serikat, Nixon menyatakan akan ada ‘ ledakan peristiwa ‘ (kepada John D. Rockefeller, yang mengawasi masalah kelebihan penduduk Afrika). Sampai saat ini pun pejabat AS antar disiplin ilmu akan membahas ‘keanehan’ hukum publik yang memberi kewenangan Amerika Serikat untuk membunuh warga negaranya sendiri dan orang lain atas nama keamanan nasional masa depan Amerika(baca : Kulit Putih). Jika Amerika Serikat berada di atas papan (gaya Manhattan), maka Presiden harus mengambil tindakan perbaikan segera untuk sepenuhnya mengungkapkan program rahasia ini.

J. Craig Venter, Jr, memegang paten untuk gen yang disebut “Afrika Amerika HIV / AIDS Entryway.” Ini adalah gen yang sama yang digunakan ilmuwan AS pada anak-anak Afrika di era 50-an (CCR5 delta 32 positif). Teori lainnya dikembangkan oleh Dr Hillary Kaprowski. AIDS menyeberang dari simpanse ke manusia ketika dokter menggunakan ginjal mereka untuk menyiapkan eksperimental vaksin oral polio (OPV). Terlepas dari bagaimana hal itu menular, kita dapat meyakini hal itu dibuat di laboratorium oleh para ilmuwan AS dan Eropa dan digunakan dalam terorisme biologis.

Gerakan Tolak ARV (GETAR), Dody Achmadi

Sumber Link : http://www.stewartsynopsis.com/boyd_ed_graves.htm

Minggu, 27 Januari 2013

Roberto Giraldo TESTS FOR HIV ARE HIGHLY INACCURATE

VIRUSMYTH HOMEPAGE

TESTS FOR HIV ARE HIGHLY INACCURATE By Roberto Giraldo June 2000

For the last 6 years I have been working at a laboratory of clinical immunology in one of the most prestigious University Hospitals in the City of New York. Here I have had the opportunity to personally run and get to know in detail the current tests used for the diagnosis of HIV status, namely, the ELISA, Western blot and Viral Load tests.
1. The ELISA, Western blot, and Viral Load tests, used for the diagnosis of "HIV infection" are not at all accurate
There are many arguments against the accuracy of these tests to diagnose infection by what is known as HIV. For those who want to search the issue deeper I strongly recommend begin studying the 1993 article in Bio/Technology by Eleni Papadopulos-Eleopulos and her group of researches from Perth, Western Australia (12).
Here are some facts that support that a person who reacts positively on these tests does not mean that he/she is infected with HIV:
1.1. The definition of AIDS, as developed by the United States Federal Government’s Centers for Disease Control and Prevention, requires a positive result on the antibody test for HIV (1). This definition is accepted worldwide. The importance of HIV in this definition is so strong that, currently, many AIDS researchers, health care professionals and lay people, in following the lead of the United States Institute of Medicine, the National Academy of Sciences and most AIDS researchers now refer to "AIDS" as "HIV Disease" (2-7).
However, AIDS in Africa can be diagnosed without HIV test or any other laboratory test. This was decided by American public health officials at a conference in Bangui, in the Central African Republic in October 1985 (WHO’s Weekly Epidemiological Record 1986; 61:69-76 and Science magazine 21 November 1986). This allows health professionals to diagnosis AIDS in Africa based only on the symptoms and signs that a patient manifests.
1.2. The tests that are used most frequently to diagnose HIV status are the ELISA "screening test", the Western blot "confirmatory test" and the PCR "Viral Load test" (8-11). In the United States the ELISA and Western blot tests, when done together, have become known as "the AIDS test". These tests supposedly detect antibodies against HIV. The "Viral Load" or PCR test is a genetic test that makes copies of small fragments of nucleic acids that, it is claimed, belong exclusively to HIV. These are the same tests that are used to check for HIV in mothers, infants, children, and in the population at large. The problem with all of these tests is that a positive HIV reaction does not guarantee that the person is really infected with HIV at all (12-21).
1.3. Currently, a positive result on "the AIDS test" - ELISA and Western blot antibody tests - is synonymous with HIV infection and the attendant risk of developing AIDS (8-11).
However, these antibody tests are neither standardized nor reproducible, with respect to HIV they are themselves meaningless because they mean different things in different individuals, they also mean different things in different laboratories and in different countries (12). They are interpreted differently in the United States, Russia, Canada, Australia, Africa, Europe and South America (22-27), which means that a person who is positive in Africa can be negative when tested in Australia; or a person who is negative in Canada can become positive when tested in Africa (28). The other problem is that the same sample of blood when tested in 19 different laboratories gets 19 different results on the Western blot test (29).
1.4. The Western blot antigens, proteins or bands - p120, p41, p32, p24/25, p17/18 - which are considered to be specific to HIV, may not be encoded by the HIV genome and may in fact represent human cellular proteins (12-14,20,30).
1.5. The only valid method of establishing the sensitivity and the specificity of a diagnostic test in clinical medicine is to compare the test in question with its gold standard. The only possible gold standard for the HIV tests is the human immunodeficiency virus itself. Since HIV has never been isolated as an independent free and purified viral entity (31), it is not possible to properly define the sensitivity or the specificity of any of the tests for HIV (12). Currently, the sensitivity and the specificity of the tests for HIV are defined not by comparison to purified HIV itself, but by comparison of the tests in question with the clinical manifestations of AIDS, or with T4 cell counts (12). Abbott states, "At present there is no recognized standard for establishing the presence and absence of HIV-1 antibody in human blood. Therefore sensitivity was computed based on the clinical diagnosis of AIDS and specificity based on random donors" (32). Since there is no gold standard for defining the specificity of the tests used for the diagnosis of HIV infection, all HIV-positive results for HIV infection must be considered false-positives.
1.6. There are abundant scientific publications explaining that there are more than 70 different documented conditions that can cause the antibody tests to react positive without an HIV infection (12-14,17,19,30). In other words, there are more than 70 scientifically acknowledged reasons for false positives when testing for HIV. This fact has been abundantly documented in the scientific literature.
1.7. Of course, it is shocking to find out that a diagnosis of HIV infection is based on tests that are not specific for HIV. However, the scientific evidence tells us that a person can react positive on the test for HIV even though he or she is not infected with HIV (12-14,17,21,30,33).
1.8. The pharmaceutical companies that make and commercialize the kits for these tests acknowledge the inaccuracy of them, and this is why the inserts that come with the kits typically state the following: "Elisa testing alone cannot be used to diagnose AIDS, even if the recommended investigation of reactive specimens suggests a high probability that the antibody to HIV-1 is present" (32). The insert for one of the kits for administering the Western blot warns, "Do not use this kit as the sole basis of diagnosis of HIV-1 infection" (34). The insert that comes with a popular kit to run viral load warns, "The amplicor HIV-1 Monitor test is not intended to be used as a screening test for HIV or as a diagnostic test to confirm the presence of HIV infection" (35). The problem is that not only most AIDS researchers, journalists and lay people but health care workers themselves do not know these facts about the tests because they do not have access to them. There likewise appears to be little or no concern on the part of the knowing faculty of institutions to communicate these facts to physicians, let alone the general public.
1.9. Since the viral load results are given in copies per ml of plasma (35) AIDS researchers, health care professionals, and lay people may think that they represent copies or counts of the virus itself (12,36-41). However, the viral load test only makes copies of fragments of nucleic acids. It does not count HIV itself. A positive viral load test cannot be regarded as signifying the presence of the whole HIV genome, and therefore the test cannot be used to measure virus.
1.10. Results of the viral load test cannot be reproduced. This can be seen in the wide range of variability that is accepted in the quality controls set by the companies that make and commercialize the test kits. For example, Roche accepts low control having a range between 1,200 and 11,000 copies per ml [Lot # 0047], and high control having a range between 99,000 and 750,000 copies per ml [Lot # A00246] [Roche, Amplicor HIV-1 Monitor test Lot # B00985, expiration August 2000]. Most important of all, the problems with the lack of a gold standard for HIV infection also apply to the evaluation of the accuracy of the PCR or Viral load test (12,41,42). As a consequence, the specificity of the viral load test for HIV has never been defined properly. Therefore, all viral load positive results are likewise false-positives for HIV.
1.11. The fact that the defenders of HIV as the cause of AIDS, had to appeal to a genetic trick – the PCR test – is a strong argument against HIV as the cause of AIDS. To have to amplify tiny amounts of genetic material in the blood of the AIDS patients to try to identify HIV, instead of culturing the entire virus, isolate it and purify it, violates one of the central rules of infectious diseases: in the climax or maximum state of severity of any infectious disease is when the patient has the higher amount of microbes in his/her tissues. Is in those moments when it is easier to isolate and purify the microbes that are really causing a disease.
1.12. People have the right to make informed choices (43-45). However, the right of informed choice implies a right to good information. There is no justification for the fact that most people have not been informed about the serious inaccuracy of the tests for HIV infection. Withholding or obscuring these facts is a serious breach of public trust, violating as it does a person’s right to informed consent when making decisions about their health care. The legal implications of this situation have been noted (46).
2. Being "HIV-positive" does not mean that a person is infected with "HIV"
2.1. There are a growing number of scientific publications explaining in detail that the tests for HIV infection are not specific for HIV (12-14,47). There are many reasons other than a past or present HIV infection to explain why an individual reacts positive on these tests. In other words these tests can react positive in the absence of HIV (12-14,17-19,30).
2.2. Some of the conditions that cause false positives on the so-called "AIDS test" are: past or present infection with a variety of bacteria, parasites, viruses, and fungi including tuberculosis, malaria, leishmaniasis, influenza, the common cold, leprosy and a history of sexually transmitted diseases; the presence of polyspecific antibodies, hypergammaglobulinemias, the presence of auto-antibodies against a variety of cells and tissues, vaccinations, and the administration of gamma globulins or immunoglobulins; the presence of auto-immune diseases like erythematous systemic lupus, sclerodermia, dermatomyositis and rheumatoid arthritis; the existence of pregnancy and multiparity; a history of rectal insemination; addiction to recreational drugs; several kidney diseases, renal failure and hemodialysis; a history of organ transplantation; presence of a variety of tumors and cancer chemotherapy; many liver diseases including alcoholic liver disease; hemophilia, blood transfusions and the administration of coagulation factor; and even the simple condition of aging, to mention a few of them (12-14,17,18,30).
2.3. It is interesting to note that all of these conditions that cause the "HIV tests" to react positive in the absence of HIV, are conditions which are present with varied distribution and concentration in all of the conventionally recognized AIDS risk groups in the developed countries, as well as in the vast majority of inhabitants of the underdeveloped world. This means that in all probability many drug users [including mothers], certain gay males, and some hemophiliacs in the developed countries, as well as the vast majority of inhabitants in most countries of Africa, Asia, South America and the Caribbean, who have positive reactions to the tests for HIV, may very well do so due to conditions other than being infected with HIV (12-14,30,48).
2.4. Further, it is well known that people with or at risk for AIDS have high levels of antibodies - immunoglobulins - as a consequence of having been exposed to significant quantities of a variety of foreign substances such as recreational drugs, semen, factor VIII, blood and blood components, sexually transmitted infections and other infections (12-14,49). All these substances are oxidizing agents that cause oxidative stress (47,50,51).
2.5. Recently I had the opportunity to carry out an experiment by which I was able to demonstrate that all blood react positively on the ELISA test when run the test with neat or non-diluted serum. This could indicate that everybody has antibodies against what is supposed to be HIV. The ones that only react positively with straight or neat serum would have fewer amount of antibodies than the ones that continue reacting positively even when the serum is diluted 400 times (88). This possibility has been confirmed by Yugoslavian and Italian researchers (90)
2.6. There is also a great deal of scientific data indicating the widespread presence of non-specific interactions between what are considered to be retroviral antigens and unrelated antibodies (12,52-54). It is then possible to conclude that the tests for HIV react positively in the presence of those antibodies; in other words, that a positive result on an antibody test for HIV may be the result of previous antigenic over-stimulation, rather than a result of an HIV or any other retroviral infection (12-14).
2.7. Finally, it has been proposed that antibodies against HIV are surrogate markers for recreational drug use in the United States and in Europe (55,56).
2.8. On the other hand, even if "the AIDS test" were able to detect antibodies to HIV, it would not be logical to say that the presence of those antibodies indicate an active infection. The presence of antibodies to any virus simply means humoral immune response to that virus and not necessarily that the virus is still active and pathogenic (48,58). One can have antibodies against many germs without those germs being active, pathogenically active or even present at all (58,59). In most instances, antibodies against viruses indicate immunity. This is the very basis of vaccination against viral diseases (48,58,60). Even if the tests were specific for antibodies against HIV, the question would then be the following: Why is it that only in the case of AIDS the presence of antibodies indicates the presence of disease, rather than protection against it?
2.9. There is no justification for the fact that both patients and the general public have had all of the preceding facts withheld from them. Without the merits and demerits of the tests for HIV, people cannot make informed decisions.
3. The so-called "AIDS virus", HIV, may not even exist
Biophysicist Eleni Papadopulos-Eleopulos and her group of researchers at Royal Perth Hospital in Perth, Western Australia, were the very first scientists in mentioning the fact that HIV has never been isolated (12). For several years Papadopulos-Eleopulos and coworkers, have been publishing papers where they have described in detail, the scientific facts that support the assertion that the so-called AIDS virus, HIV, may not even exist (12-14,20,30,31,47,50,61-64):
3.1. The correct procedures (31) employed for over half a century to achieve isolation of a retrovirus are: a) to find in infected cell cultures particles with a diameter of 100-120 nM that contain the so-called condensed inner bodies or cores and that have surfaces studded with projections - spikes, knobs - b) In sucrose density gradients the particles band at a density of 1.16 gm/ml; c) At the density of 1.16 gm/ml there is nothing else but particles with the morphological characteristics of retroviral particles; d) The particles contain only RNA and not DNA, and the RNA consistently has the same length [number of bases] and composition no matter how many times the experiment is repeated; e) When the particles are introduced into secondary cultures they are taken up by the cells, the entire RNA is reverse transcribed into cDNA, the entire cDNA is inserted into the cellular DNA, and the DNA is transcribed back into RNA which is then translated into proteins; f) As a result of e the cells in the secondary cultures release particles into the culture medium; g) The particles released into the secondary culture medium have exactly the same characteristics as the original particles, that is, they must have identical morphology, band at 1.16 gm/ml and contain the same RNA and proteins (31).
None of these procedures have been achieved in the case of HIV (12,14,31,47).
3.2. None of the researchers who claim to have isolated HIV have shown the presence of particles with the morphological characteristics of retroviruses banding at 1.16 gm/ml (31).
Even the word "isolation" as used by the most noted researchers (65-67) is incorrect and misleading since neither Montagnier, Gallo nor Levy isolated HIV particles, particles of any other human retrovirus, or even virus-like-particles at all (12-14,30,31,47,61,68-74).
3.3. Since no "retroviral particles" [retroviruses] have ever been isolated from any culture (12-14,31,47,61-63,69-75), the existence of HIV has been established indirectly: by the presence in blood cultures of AIDS and "HIV-positive" individuals, proteins/glycoproteins such as gp 160/150, gp120, gp41/45/40, p34/32, p24, and p18/17, each claimed to belong to HIV; by the presence of enzymes such as reverse transcriptase that supposedly belongs to HIV; and by the presence of RNA or DNA fragments that supposedly belong to HIV (12-14,31,47,61-63,69-75).
However, none of these substances have been proven to belong to HIV at all (12-14,31,47,61-63,69-75). How can anybody prove that the substances found in those cultures belong to a viral particle that has never been found at 1.16 gm/ml? To prove that those substances are part of a retrovirus named HIV, it is absolutely necessary that the retroviral particles have been previously separated - isolated - from everything else. This has never been done with HIV (31).
3.4. It is interesting to note that the substances listed in 6.3. are claimed to appear exclusively when one co-cultures supposedly infected blood with abnormal cells from leukemia patients, or from umbilical cord lymphocytes (31). The problem is that the same substances can be obtained from the same cultures in the absence of the supposedly HIV-infected blood (31).
3.5. The cultures where the above substances have been found are cultures that have been heavily stimulated with substances such as phytohemagglutinin, IL-2, antiserum to human interferon, and other agents (31). These culture stimulants are oxidizing agents (31,47). The problem is that the same type of material can be observed in stimulated cultures of lymphocytes from healthy persons (31,76).
It is interesting to note than in the presence of antioxidants, no HIV phenomena can be observed in culture; nor can HIV substances be found (12,64,76).
3.6. The substances listed in 6.3. are not specific to HIV at all (31). For instance, it is currently known that reverse transcriptase can be found associated with entities other than retroviruses, including eukaryote cells, some animal and plant DNA viruses, and even some introns (77).
Gallo and co-workers have claimed that the cell-free supernatants from "infected" cultures have HIV-DNA (78,79). They forgot that by definition retroviruses are infectious particles that contain only RNA. When retroviruses enter a cell the RNA is reverse transcribed into DNA, which is then integrated into cellular DNA as a provirus, which means that "HIV DNA" will be present only in the cell and no where else (31).
There is also ample evidence that any RNA or DNA present in the supernatant of the cultures is there as an effect of stimulation by polycations and oxidizing agents, rather than as an effect of the presence of a retrovirus (31).
"HIV cloning" is likewise misleading. Without isolating a retroviral particle containing RNA inside its core, the cloning of that "specific HIV-RNA" is not possible (31).
3.7. To date nobody has presented evidence that the so-called HIV proteins or antigens [gp160/150, gp120, gp41/45/40, p34/32, p24, p18/17], are constituents of a retrovirus particle or even retrovirus-like particle let alone a unique retrovirus, HIV (31).
3.8. The proteins or antigens derived from stimulated cultures form the basis for the ELISA and Western blot HIV antibody tests (31,73). Fragments of RNA from stimulated cultures form the basis of the HIV viral load test (31,73). This is the main reason why the current tests used for the diagnosis of HIV are not specific for it (12-14,31,61,62).
3.9. In the January 1997 issue of the journal Virology, two independent groups of researchers published experiments claiming to isolate HIV. Now and for the first time in the history of HIV, the researchers followed the internationally accepted procedures to isolate retroviral particles. Not surprisingly, in the sedimented bands at 1.16 gm/ml of sucrose, where retroviruses are known to be located, nothing was found but cellular debris. At 1.16 gm/ml there was nothing that even looked like a retroviral particle (80-81). They could not have isolated HIV simply because HIV was not there to be isolated.
It has been proposed that all those substances that indicate the existence of HIV are nothing more than non-viral material altogether, induced by the agents to which the AIDS patients and cultures are exposed (31). When found in people, these substances would be seen as regular products of the stress response (82), secondary to exposure to chemical, physical, biological, mental, and nutritional stressor agents (48,51,57,83-87).
3.10. It is therefore possible to conclude that the entire model of AIDS as an infectious and transmissible viral disease has its basis on a non-existing organism. The foundation stone for the HIV-AIDS model then, is a ghost.
4. The real meaning of being HIV-positive
4.1. Above considerations allow one to propose that the reactivity on the ELISA, Western blot, and PCR tests is caused by multiple, repeated, and chronic exposure to chemical, physical, biological, mental, and nutritional stressor agents. The degree of reactivity would be proportional to the level of exposures to immunological stressor or oxidizing agents (12-14,20,30,31,63,88,89).
Positive results on ELISA and Western blot tests, can also be understood as the consequence of the presence of high levels of polyspecific antibodies, due to a state of chronic polyantigenic stimulation (52-54). The reactivity on the three main tests for HIV -ELISA, Western blot, and PCR or viral load - would be simply the result of the stress response (82,88,89,91-94).
4.2. Being "HIV-positive" - reacting positive on the tests for HIV – would then mean simply that the person has been exposed to many antigenic and toxic challenges, i.e., to many oxidizing agents (47,50,89). His or her immune system has been responding a lot to these immunogenic and immunotoxic challenges (51,57,89). The immune system of these "HIV-positive" individuals would be debilitated - oxidized - after it has been over-stimulated and intoxicated. Therefore, their risk for AIDS is higher than those who are "HIV-negative" (12,13,49,51).
4.3. Undoubtedly, there is almost a perfect correlation between the reactivity on the so-called "tests for HIV" and AIDS.
Exposure to immunological stressors makes the tests to react positively. At the same time, the exposure to immunological stressors or oxidizing agents is the cause of the mild to moderate levels of immune suppression present in all non-symptomatic individuals who react positively on the "tests for HIV." If the exposure to immunological stressor is not stopped, and if the individual is not disintoxicated, it is very probably that the non-symptomatic "HIV-positive" individual will worsen his/her immune suppression, and will develop the clinical manifestations of AIDS.
What we know as HIV has not causative role in AIDS. By the contrary, the HIV phenomenon is one of the effects of the stress response to multiple repeated, and chronic exposures to chemical, physical, biological, mental, and nutritional stressor agents.
5. Possible trial to find out the real meaning of the tests for HIV
To take blood from four groups of people and run the tests highly diluted, undiluted and at a wide spectrum of dilutions in between. a) The first group would be a group of healthy people of many age groups, b) the second group would be a group of people from the conventional AIDS risk groups, c) the third group would be a group of people with clinical conditions unrelated to AIDS, and d) the fourth group would be a group of patients with full manifestations of AIDS.
All groups would be subjected to both ELISA and Western blot tests. Additionally, all blood samples could be subjected to the viral load test for HIV.
The result of such experiment could determine whether these tests measurements bear any relationship to an individual’s level of exposure to stressor or oxidizing agents. If so, the tests could be salvaged as a measure of individual’s level of intoxication.

This article was written in June 2000 and posted during the Internet Discussion of the South African Presidential AIDS Advisory Panel
References

CDC. Centers for Disease Control and Prevention. 1993 Revised Classification System for HIV Infection & Expanded Surveillance Case Definition for AIDS Among Adolescents & Adults. MMWR 1992; 41: 1-19.

FAUCI AS. Immunopathogenesis of HIV Infection. J Acq Immunodeficiency Syndromes 1993: 6:655-662.

STAPRANS SI and FEINBERG MB. Natural History and Immunopathogenesis of HIV-1 Disease. In: SANDE MA and VOLBERDING PA. The Medical Management of AIDS. 5^th Edition. Philadelphia: W.B. Saunders Company, 1997: 29-56.

LEVY JA. Overal Features of HIV Pathogenesis: Prognosis for Long-Term Survival. In: HIV and the Pathogenesis of AIDS. Second Edition. Washington DC: ASM Press, 1998: 311-338.

VOLBERDING PA and COHEN PT. Natural History, Clinical Spectrum, and General Management of HIV Disease. In: COHEN PT, SANDE MA and VOLBERDING PA. The AIDS Knowledge Base. Boston: Little, Brown and Company, 1994: Section 4.

INSTITUTE OF MEDICINE & NATIONAL ACADEMY OF SCIENCES. Confronting AIDS. Washington DC: National Academy Press, 1986.

WORTLEY PM, CHU SY and BERKELMAN RL. Epidemiology of HIV/AIDS in Women and Impact of the Expanded 1993 CDC Surveillance Definition of AIDS. In: COTTON D and WATTS DH. The Medical Management of AIDS in Women. New York: John Wiley & Sons, 1997: 3-14.

FEINBERG MA and VOLBERDING PA. Testing for Human Immunodeficiency Virus. In: COHEN PT, SANDE MA and VOLBERDING PA. The Aids Knowledge Base. Boston: Little, Brown and Company, 1994: Section 2.

PINS MR, TERUYA J and STOWELL CP. Human Immunodeficiency Virus Testing and Case Detection: Pragmatic and Technical Issues. In: COTTON D and WATTS DH. The Medical Management of AIDS in Women. New York: John Wiley & Sons, 1997: 163-176.

METCALF JA, DAVEY RT and LANE HC. Acquired Immunodeficiency Syndrome: Serologic and Virologic Tests. In: DEVITA VT, CURRAN J, HELLMAN S, et al. AIDS: Etiology, Diagnosis, Treatment and Prevention. 4^th Edition. Philadelphia: Lippincott - Raven, 1997: 177-196.

WEISS SH. Laboratory Detection of Human Retroviral Infection. In: WORMSER GP. AIDS and Other Manifestations of HIV Infection. New York: Lippincott- Raven, 1998: 175-200.

PAPADOPULOS-ELEOPULOS E, TURNER V & PAPADIMITRIOU JM. Is a Positive Western Blot Proof of HIV Infection ? Bio/Technology 1993; 11:696-707.

PAPADOPULOS-ELEOPULOS E, TURNER V, PAPADIMITRIOU J & CAUSER D. HIV Antibodies: Further Questions and a Plea for Clarification. Curr Med Res Opin 1997; 13:627-634.

PAPADOPULOS-ELEOPULOS E, TURNER V, PAPADIMITRIOU J, et al. Why No Whole Virus? Continuum (London) 1997; 4(5):27-30.

JOHNSON C. Playing Russian Roulete in the Lab: Can you Really Trust the AIDS Test? New York: The HEAL Bulletin, Special Edition, 1993.

JOHNSON C. Is Anyone Really Positive? Continuum (London); April/May 1995.

JOHNSON C. Factors Known to Cause False-Positive HIV Antibody Test Results; Zenger’s San Diego, California, September 1996: 8-9.

JOHNSON C. Whose Antibodies Are They Anyway? Continuum (London), September/October 1996; 4(3):4-5.

HODGKINSON N. Science Fails the "AIDS Test". In: AIDS: The Failure of Contemporary Science. How a Virus that Never Was Deceived the World. London: Fourth Estate, 1996: 232-262.

TURNER VF. Do HIV Antibody Tests Prove HIV Infection? Continuum (London) 1996; 3:8-11.

BAUMGARTNER M and The International Forum for Accessible Science. Information Dosier: United Nations Commission on Human Rights, Geneva, Switzerland. April 1998: 64.

CDC. Centers for Disease Control and Prevention. Interpretation and Use of the Western Blot Assay For Serodiagnosis of Human Immunodeficiency Virus Type 1 Infections. MMWR 1989; 38 :S1-S7.

ZOLLA-PAZNER S, GORNY MK & HONNEN WJ. Reinterpretation of Human Immunodeficiency Virus Western Blot Patterns. NEJM 1989; 320:1280-1281.

BURKE DS. Laboratory Diagnosis of Human Immunodeficiency Virus Infection. Clin Lab Med 1989; 9:369-392.

DE COCK KM, SELIK RM, SORO B, et al. AIDS Surveillance in Africa: A Reappraisal of Case Definition. BMJ 1991; 303:1185-1189.

MASKILL WJ & GUST ID. HIV-1 Testing in Australia. Australian Prescriber 1992; 15:11-13.

VOEVODIN A. HIV Screening in Russia. Lancet 1992; 399:1548.

CONTINUUM. HIV Positive ? - It Depends Where You Live. Take a Look at the Criteria that Determine a Positive HIV Test Result. Continuum (London) 1995; 3(4):20.

LUNDBERG GD. Serological Diagnosis of Human Immunodeficiency Virus Infection by Western Blot Testing. JAMA 1988; 260:674-679.

TURNER VF. Do Antibody Tests Prove HIV Infection?. Interview by Huw Christie editor of Continuum. Continuum (London) Winter 1997/8; 5(2):10-19.

PAPADOPULOS-ELEOPULOS E, TURNER VF, PAPADIMITRIOU JM & CAUSER D. The Isolation of HIV: Has it Really Been Achieved? The Case Against. Continuum (London) 1996; 4(3): S1-S24.

ABBOTT LABORATORIES. Human Immunodeficiency Virus Type 1. HIVAB HIV-1 EIA. Abbott Laboratories, Diagnostics Division. January, 1997 (66-8805/R5), 5 pages.

BUIANOUCKAS FR. HEAL’s Alternative AIDS Test. A Practical Alternative to T-Cell and Antibody Tests. HEAL (Health Education AIDS Liaison) Comprehensive Packet 1993.

EPITOPE, ORGANON TEKNIKA. Human Immunodeficiency Virus Type 1 (HIV-1). HIV-1 Western Blot Kit. PN201-3039 Revision # 6, page 11.

ROCHE. Amplicor HIV-1 Monitor test. Roche Diagnostic Systems, 13-06-83088-001, 06/96.

PIATAK N, SAAG MS, YANG LC, et al. High Levels of HIV-1 in Plasma During All Stages of Infection Determined by Competitice PCR. Science 1993; 259:1749-1754.

VAN GEMEN B, KIEVITS T, SCHUKKINK R, et al. Quantification of HIV-1 RNA in Plasma Using NASBA During HIV-1 Primary Infection. J Virol Meth 1993; 43:177-188.

KWOK S & SPINSKY JJ. PCR Detection of Human Immunodeficiency Virus Type 1 Proviral DNA Sequences. In: PERSING DH, SMITH TF, SMITH FC, et al. (eds.) Diagnostic Molecular Biology: Principles and Applications. Washington DC:ASM Press, 1993.

MULDER J, MCKINNEY N, CRISTOPHERSON C, et al. Rapid and Simple PCR Assay for Quantitation of Human Immunodeficiency Virus Type 1 RNA in Plasma: Application to Acute Retroviral Infection. J Clin Microbiol 1994; 32:292-300.

DEWAR RL, HIGBARGER HC, SARMIENTO MB, et al. Application of Branched DNA Signal Amplification to Monitor Human Immunodeficiency Virus Type 1 Burden in Human Plasma. J Inf Dis 1994; 170:1172-1179.

JOHNSON C. The PCR to Prove HIV Infection. Viral Load and Why They Can’t Be Used. Continuum (London) 1996; 4:33-37 and 39.

PHILPOTT P & JOHNSON C. Viral Load of Crap. Reappraising AIDS 1996; 4(10):1-4.

KENT G, DELANY L, HOPE T and GRANT V. Teaching Analysis. Informed Consent: A Case for Multidisciplinary Teaching. Health Care Analysis 1996; 4(1):65-79.

O’MARA P. Life, Liberty, and Informed Consent. Mothering September/October 1998; (90): 6-9.

SILVERMAN WA. Informing and Consenting. In: Where’s The Evidence ? Controversies in Modern Medicine.Oxford: Oxford University Press, 1998: 78-84.

CHRISTIE H. Wake the Law. Damaging, Non-Specific HIV Testing at the Hands of the Medical Industry Must Soon Prompt Large Finantial Compensation for "the Diagnosed" It’s Time to Sue! Continuum (London) Spring 1998; 5(3):28-29

PAPADOPULOS-ELEOPULOS E. Reappraisal of AIDS - Is the Oxidation Induced by the Risk Factors the Primary Cause? Medical Hypothesis 1988; 25:151-162.

GIRALDO RA. AIDS and Stressors IV: The Real Meaning of HIV. In: AIDS and Stressors. Medellín, Colombia: Impresos Begón, 1997: 133-173.

SHALLENBERGER F. Selective Compartmental Dominance: An Explanation for a Nonifectious, Multifactorial Etiology for Acquired Immune Deficiency Syndrome (AIDS), and a Rationale for Ozone Therapy and other Immune Modulating Therapies. Med Hypothesis 1998; 50:67-80.

TURNER VF. Reducing Agents and AIDS - Why Are We Waiting? Med J Austr 1990; 153:502.

GIRALDO RA. AIDS and Stressors II: A Proposal for the Pathogenesis of AIDS. In: AIDS and Stressors. Medellín: Impresos Begón, 1997: 57-96.

SNYDER HW and FLEISSNER E. Specificity of Human Antibodies to Oncovirus Glycoproteins: Recognition of Antigen by Natural Antibodies Directed Against Carbohydrate Structures. Proc Nat Acad Sci USA 1980; 77:1622-1626.

BARBACID M, BOLAGNESI D & AARONSON SA. 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 Nat Acad Sci USA 1980; 77:1627-1621.

WING MG. The Molecular Basis for a Polyspecific Antibody. Clin Exp Immunol 1995; 99:313-315.

DUESBERG PH. AIDS Acquired by Drug Consumption and other Non Contagious Risk Factors. Pharmac Ther 1992; 55:201-277.

DUESBERG PH & RASNICK D. The Drug-AIDS Hypothesis. Continuum (London) 1997; 4(5):S1-S24.

GIRALDO RA. AIDS and Stressors III: A Proposal for the Natural History of AIDS. In: AIDS and Stressors. Medellín: Impresos Begón, 1997: 97-131.

ZINKERNAGEL RM. Immunity to Viruses. In: PAUL WE. Fundamental Immunology. Third Edition. New York: Raven Press, 1993: 1211-1250.

MIMS CA, DIMMOCK NJ, NASH A & STEPHEN J. The Immune Response to Infections. In: Mims’ Pathogenesis of Infectious Diseases. Chapter 6. London: Academic Press, 1995: 136-167.

EVANS AS. Viral Infections of Humans, Epidemiology and Control. New York: Plenum Publishing Corporation, 1989.

PAPADOPULOS-ELEOPULOS E. Is HIV the Cause of AIDS. Interview by Christine Johnson. Continuum (London) 1997; 5(1):8-19.

PAPADOPULOS-ELEOPULOS E, TURNER V, PAPADIMITRIOU J, et al. Between the Lines. A Critical Analysis of Luc Montagnier’s Interview Answers to Djamel Tahi. Continuum (London) 1997/8; 5(2):35-45.

TURNER VF. Where Have We Gone Wrong? Continuum (London) 1998; 5(3):38-44.

PAPADOPULOS-ELEOPULOS E, TURNER V & PAPADIMITRIOU J. Oxidative Stress, HIV and AIDS. Res Immunol 1992; 143:145-148.

BARRE-SINOUSSI F, CHERMANN JC, REY F et al. Isolation of a T-Lymphotropic Retrovirus from a Patient at Risk for Acquired Immune Deficiency Syndrome (AIDS) Science 1983; 220:868-871.

PAPOVIC M, SARNGADHARAN MG, READ E, et al. Detection, Isolation, and Continious Production of Cytopathic Retroviruses (HTLV-III) from Patients with AIDS and Pre-AIDS. Science 1984; 224:497-500.

LEVY J, HOFFMAN AD, KRAMER SM, et al. Isolation of Lymphocytopathic Retroviruses from San Francisco Patients with AIDS. Science 1984; 225:840-842.

BUIANOUCKAS FR. HIV an Illusion. Nature 1995; 375:197.

LANKA S. HIV: Reality or Artefact? Continuum (London) 1995.

LANKA S. Collective Fallacy. Rethinking HIV. Continuum (London) 1996; 4(3):19-20.

LANKA S. No Viral Identification: No Cloning as Proof of Isolation. Continuum (London) 1997; 4(5):31-33.

DE HARVEN E. Pioneer Deplores "HIV" "Maintaining Errors is Evil" Continuum (London) 1997/8; 5(2):24.

DE HARVEN E. Remarks on Methods for Retroviral Isolation. Continuum (London) 1998; 5(3):20-21.

PHILPOTT P. The Isolation Question. Does HIV Exist? Do HIV Tests Indicate HIV Infection? Here’s Why Some Scientists Say No. How an Australian Biophysicist and her Simple Observations Have Taken Center Stage Among AIDS Reappraisers. Reappraising AIDS 1997; 5(6):1-12.

HODGKINSON N.Origin of the Specious. Continuum (London) 1996c; 4(3):17-18.

KLATZMANN D & MONTAGNIER L. Approaches to AIDS Therapy. Nature 1986; 319:10-11.

DOOLITTLE RF, FENG DF, JOHNSON MS, et al. Origins and Evolutionary Relationships of Retroviruses. Quart Rev Biol 1989; 64:1-30.

LORI D, DI MARZO VERONESE F, DE VICO AL, et al. Viral DNA Carried by Human Immunodeficiency Virus Type 1 Virions. J Virol 1992; 66:5067-5074.

ZHANG H, ZHANG Y, SPICER TS, et al. Reverse Transcription Takes Place Within Extracellular HIV-1 Virions: Potential Biological Significance. AIDS Res Hum Retrovirus 1993; 9:1287-1296.

GLUSCHANKOF P, MONDOR I, GELDERBLOM HR, et al. Cell Membrane Vesicles are a Major Contaminant of Gradient-Enriched Human Immunodeficiency Virus Type-1 Preparations. Virology 1997; 230:125-133.

BESS JW, GORELICK RJ, BOSCHE WJ, et al. Microvesicles are a Source of Contaminating Cellular Proteins Found in Purified HIV-1 Preparations. Virology 1997; 230:134-144.

KOVAL TM. Stress-Inducible Processes in Higher Eukaryotic Cells. New York: Plenum Press, 1997: 256.

GIRALDO RA. AIDS and Stressors I: Worldwide Rise of Immunological Stressors. In: AIDS and Stressors. Medellín: Impresos Begón, 1997: 23-56.

GIRALDO RA. Polemica Cientifica Internacional Acerca de la Causa del SIDA. Investigacion y Educacion en Enfermeria (University of Antioquia, Colombia) 1996; 14(2):55-74.

GIRALDO RA. Papel de Estresantes Inmunologicos en Inmunodeficiencia. IATREIA (University of Antioquia, School of Medicine, Colombia) 1997; 10:62-76.

GIRALDO RA. AIDS and Stressors: AIDS in Neither an Infectious Disease nor is Sexually Transmitted. It is a Toxic-Nutritional Syndrome Caused by the Alarming Worldwide Increment of Immunological Stressor Agents. Medellín, Colombia: Impresos Begón, 1997: 205.

GIRALDO RA. AIDS in Neither an Infectious Disease nor is Sexually Transmitted. In: AIDS and Stressors. Medellín: Impresos Begón, 1997: 175-187.

GIRALDO RA. Everybody Reacts Positive on the ELISA Test for HIV. Continuum (London) 1999; 5(5):8-10.

GIRALDO RA, ELLNER M, FARBER C, et al. Is it Rational to Treat or Prevent AIDS with Toxic Antiretroviral Drugs in Pregnant Women, Infants, Children, and Anybody Else? The Answer is Negative. Continuum (London) 1999; 5(6): 38-52.

METLAS R, et al. Human Immunodeficiency Virus V3 Peptide-Reactive Antibodies are Present in Normal HIV-Negative Sera. AIDS Research and Human Retroviruses 1999; 15: 671-677.

MORIMOTO R, TISSIERES A, GEORGOPOULOS C. Stress Proteins in Biology and Medicine. Cold Spring Harbor Laboratory Press 1990: 450.

SCHLESINGER MJ, SANTORO MG, GARACI E. Stress Proteins: Induction and Function. Berlin: Springer-Verlag 1990: 123.

VAN EDEN W, YOUNG DB. Stress Proteins in Medicine. New York: Marcel Dekker, Inc. 1996: 578.

LATCHMAN DS. Stress Proteins. Springer, 1999: 422

VIRUSMYTH HOMEPAGE

Pembuat alat test HIV bahwa alat test mereka tidak dapat diandalkan

Health Education AIDS Liaison, Toronto

TEST KIT MANUFACTURERS ADMIT THEIR
"HIV TESTS" ARE UNRELIABLE

The following are more excerpts from the instruction pamphlets that come with the most commonly used HIV antibody tests (emphasis is ours):

[Abbott Laboratories] HIVABtm HIV-1 EIA "SUMMARY AND EXPLANATION OF THE TEST... The prevalence of HIV-1 infection in people not known to be at increased risk is not known. The HIV-1 antibody enzyme-linked immunassay (EIA) (the abbreviation "ELISA" is equally acceptable) was developed to detect antibodies to HIV-1 and was developed to identify potentially infectious units of donated blood and plasma. It has been established that repeatably reactive units of blood and plasma should be eliminated from the blood supply.
In order to afford maximum protection of the blood supply, the EIA was designed to be extremely sensitive. As a result, non-specific reactions may be seen in samples from some people, who, for example, due to prior pregnancy, blood transfusion, or other exposure, have antibodies to the human cells or media in which the HIV-1 is grown for manufacture of the EIA. Because of these and other nonspecific reactions, it is appropriate to investigate specimens found to be reactive on EIA in a manner that gives improved predictability that HIV-1 antibody, in fact is present.When a specimen reacts in an initial test (is initially reactive), the EIA should be repeated in duplicate on the same sample source. Reactivity in either or both of these duplicate tests (repeatably reactive) is highly predictive of the presence of antibody in people at increased risk for HIV-1 infection (e.g., homosexual men, hemophiliacs, or intravenous drug users). Repeatedly reactive specimens obtained from people at increased risk for HIV-1 infection are usually found to contain antibodies by additional more specific, or supplemental, testing. However, when the EIA is used to screen populations in which the prevalence of HIV-1 infection is low (e.g., blood donors), nonspecific reactions may be more common ....
... Although for all clinical and public health applications of the EIA boththe degree of risk for HIV-1 infection of the person studied and the degree of reactivity of the serum may be of value in interpreting the test, these correlations are imperfect. Therefore, in most settings it is appropriate to investigate repeatedly reactive specimens by additional more specific, or supplemental tests."*
"LIMITATIONS OF THE PROCEDURE (of ELISA)
The [Abbot Laboratories] HIVAB HIV-1 EIA antibody procedure and the Interpretation of Results must be followed closely when testing for the presence of antibodies to HIV-1 in plasma or serum from individual subjects. Because the EIA was designed to test individual units of blood or plasma, most data regarding its interpretation were derived from testing individual samples. Insufficient data are available to interpret tests performed on other body specimens, pooled blood or processed plasma, and products made from such pools: testing of these specimens is not recommended.
[Abbot Laboratories] HIVAB HIV-1 EIA detects antibodies to HIV-1 in blood and thus is useful in screening blood and plasma donated for transfusion and further manufacture, in evaluating patients with signs or symptoms of AIDS, and in establishing prior infection with HIV- 1. Clinical studies continue to clarify and refine the interpretation and medical significance of the presence of antibodies to HIV-1. For most uses it is recommended that repeatably reactive specimens be investigated by an additional more specific, or supplemental test. A person who has antibodies to HIV-1 is presumed to be infected with the virus, except that a person who has participated in an HIV vaccine study may develop antibodies to the vaccine and may or may not be infected with HIV. Clinical correlation is indicated with appropriate counseling, medical evaluation and possible additional testing to decide whether a diagnosis of HIV infection is accurate. Such an evaluation should be considered an important part of HIV-1 antibody testing and should include test result confirmation on a freshly drawn sample.**
AIDS and AIDS-related conditions are clinical syndromes and their diagnosis can only be established clinically. EIA testing alone cannot be used to diagnose AIDS, even if the recommended investigation of reactive specimens suggests a high probability that the antibody to HIV-1 is present. A negative test result at any point in the investigation of individual subjects does not preclude the possibility of exposure to or infection with HIV-1. The risk of an asymptomatic person with a repeatably reactive serum sample developing AIDS or an AIDS-related condition is not known.***
Data obtained from testing persons both at increased and at low risk for HIV-1 infection suggest that repeatably reactive specimens with high absorbance on EIA are more likely to demonstrate the presence of the HIV-1 antibodies by additional more specific, or supplemental testing. Reactivity at or only slightly above the cut-off value is more frequently nonspecific, especially in samples obtained from persons at low risk for HIV-1 infection; however, the presence of antibodies in some of these specimens can be demonstrated by additional more specific, or supplemental testing."
"Sensitivity and Specificity
At present there is no recognized standard for establishing the presence and absence of HIV-1 antibody in human blood.Therefore sensitivity was computed based on the clinical diagnosis of AIDS and specificity based on random donors.
The ABBOT studies show that:

Sensitivity based on an assumed 100% prevalence of HIV-1 antibody in AIDS patients is estimated to be 100% (144 patients tested).
Specificity based on an assumed zero prevalence of HIV-1 antibody in random donors is estimated to be 99.9% (4777 random donors tested)."

COMMENTARY:
* It is a most disturbing situation that initially indeterminate test results are routinely "interpreted" negative or positive depending on the degree of risk of the person tested. In Ontario's testing laboratories one third of test results are indeterminate.
** One should ask why antibodies induced by a vaccine would be protective when HIV antibodies otherwise are consider not protective?; or conversely, if HIV antibodies induced by vaccine are protective why wouldn't they otherwise be generally protective?
*** This comes very close to saying that the only way to be reasonably certain that an HIV antibody test result is true positive is the appearance of the clinical syndrome. This presents flawed circular logic; as AIDS has no unique symptoms but is a syndrome of up to 29 old diseases, cases can only be confirmed as AIDS by an HIV antibody positive test result. Both the syndrome and the test, each doubting their own validity, rely on each other for support.

Now from the test to confirm the above test:

HIV-1 Western Blot Kit
Epitope, Inc. Product Number 72827
PN201-3039 Revision #8 "SUMMARY AND EXPLANATION OF THE TESTA sample that is reactive in both the EIA screening test and the Western blot is presumed to be positive for antibody to HIV-1, indicating infection with this virus except in situations of passively acquired antibody or experimental vaccination."
"LIMITATIONS OF THE PROCEDURE
1. The assay must be performed in strict accordance with these instructions to obtain accurate, reproducible results.
2. Although a Positive result may indicate infection with the HIV-1 virus, a diagnosis of Acquired Immunodeficiency Syndrome (AIDS) can be made only if an individual meets the case definition of AIDS established by the Centers for Disease Control.A repeat test on an independent sample should be considered to control for sample mix-up or operator error, and to verify a positive test result.
3. Individuals with HIV-1 infection may present incomplete patterns due to the natural history of AIDS or other immunodeficiency states, e.g.:
a. AIDS patients may lose antibody reactions to p24 & p31;
b. Infants born to HIV-1 infected mothers, but who are uninfected, may display incomplete patterns as passively acquired maternal antibodies begin to disappear ;
c. Individuals who have recently seroconverted may display incomplete band patterns;
d. Infected patients with malignancies and individuals receiving immunosuppressive drugs may fail to develop a Positive result;
e. Individuals infected with HTLV-I/II or HIV-2, may exhibit incomplete cross-reactivity;
f. Individuals may develop incomplete patterns that reflect the composition of experimental HIV sub-unit vacines that they may have received.
[...]
5. Since reactivity of any degree with any of the virus-specific proteins identified on the strip is possible evidence of antibodies to HIV-1, all samples interpreted as Indeterminate should be repeated using the original specimen. In addition, it is recommended that samples interpreted as Indeterminate be retested after six months, using a fresh specimen.
6. Do not use this kit as the sole basis of diagnosis of HIV-1 infection. 7. A Negative result does not exclude the possibility of HIV-1 infection. Antibody testing should not be used in lieu of donor self-exclusion by blood collection establishments."
Sensitivity and Specificity
Sensitivity and specificity of the HIV-1 Western Blot Kit was determined in comparative studies with a previously licenced HIV-1 Western blot using EIA repeatedly reactive samples from high AIDS risk and low risk populations respectively."*
"INTERFERING FACTORS AND SUBSTANCES
Testing was performed on specimens from individuals with clinical conditions unrelated to HIV-1 which might result in a reactivity with proteins present. Samples studied included 25 from persons with auto immune diseases, 12 with elevated gammaglobulins, 110 with viral infections unrelated to HIV-1 and 38 other conditions. The viral infections included samples positive in clinical tests for Cytomegalovirus (12), Infectious mononucleosis (10), Epstein-Barr virus (3), Rubells (12), Varcella-Zoster (3), Herpes Simplex (12), HBsAg (7), and HTLV-1 (39). Although bands were occasionally present at viral locations, none of the strips could be interpreted as positive."**

COMMENTARY:
* Although the Western Blot is supposed to be a "more specific" test to confirm the results of the EIA (ELISA), the specificity and sensitivity are assumed by the same indirect means. No gold standard was applied, such as isolating HIV-1 from fresh patient plasma, in any of these studies. These studies confuse specificity with a high reproducibility of EIA by Western Blot.
** The samples studied to establish whether false positives resulted from interfering factors appear to represent individuals with isolated incidents of these factors. Even so, 38% had reactions on one or more "viral" bands of the Western Blot. People at risk for AIDS typically have accumulated many of these factors. One would assume that this would lead to higher reactivity on the Western Blot. This presents a catch 22 situation: these factors may be the cause of AIDS-like syndromes but are considered HIV-1 related because the patients react positive on EIA and Western Blot tests.

So what is the story with PCR "viral load" tests?

The AMPLICOR HIV-1 MONITOR test is an in vivo nucleic acid amplification test for the quantification of Human Immunodeficiency Virus Type 1 (HIV-1) in human plasma. The test is intended for use in conjunction with clinical presentation and other laboratory markers as an indicator of disease prognosis.The test has been used as an aid in assessing viral response to antiretroviral treatment as measured by changes in plasma HIV-1 RNA levels. The clinical significance of changes in HIV RNA measurements has not been fully established although several large studies that will more fully determine the role of comparative HIV RNA measurements in patient management are now in progress. HIV-1 RNA levels as measured by PCR were used as one of the surrogate markers in the accelerated approval process for the protease inhibitor drugs INVIRASE, CRIXIVAN and NORVIR, and for the reverse transcriptase inhibitor drug EPIVIR. The utility of plasma HIV-1 RNA in surrogate endpoint determinations has not been fully established.
The AMPLICOR HIV-1 MONITOR Test is not intended to be used as a screening test for HIV or as a diagnostic test to confirm the presence of HIV infection.

CERTIFICATE OF ACCURACY
Should a physician insist that you, or your child, test, insist that they first sign this document. If they are certain that HIV tests are accurate, they should agree without hesitation to stand behind their recommendations and provide, in writing, their assurance for your health and safety.