should i have sex with my boyfriend? he has AIDS.?

Question

i really love my boyfriend and want to spend the rest of my life with him. but i dont want to get AIDS. i am really unsure about this...

oh yeah, i forgot to mention that i am young, young meaning not old enough to drive yet.

Answer 1

Go for it, if you really love him. I think it's a great idea, shows real solidarity with him. Just no kissing, and make sure you both wear protection.

Answer 2

ok honey if you r willing to die for this man then and i hope you have done everything in life you ever wanted to do then by all means go 4 it but if this is just a couple of mts then hell no what r u crazy if you r young no no no no what r you thinking. remeber when you get this disease it will be hard for you in life life alreadt hard so you need to sit and think about what life means to you and if you want children or if you have children how life is going to be 4 them.

Answer 3

that is so high risk! safe sex is a joke - there is no such thing. the chance of pregnancy or contracting VD is always there. i can't believe you would consider having sex with someone who has AIDS! would you eat contaminated food if he asked you to?

Answer 4

You can't have your cake and eat it too. Either use protection and accept that you still might get it or don't have sex with him. It really is that simple.

Answer 5

no !!! unless you really are going to spend the rest of your life with him as in you are on your honeymoon , no - why risk your life?

Answer 6

sure while your at go ahead and share dirty needles with too. and then why dont you take a loaded gun and low your brains out.

Answer 7

i wouldnt,,, but if you do,, make sure your safe

Answer 8

no you could die if you do

Answer 9

NO NO NO

Answer 10

"The Evidence That HIV Causes AIDS", is a document that was created by the Office of Communications and Public Liaison of the National Institute of Allergy and Infectious Diseases/National Institutes of Health (NIAID/NIH): www.niaid.nih.gov/factsheets/evidhiv.htm (November 1994, updated on November 29, 2000). It is the most comprehensive document we know of to attempt to answer the many arguments that HIV does not cause AIDS. In the following rebuttal we argue that the NIAID/NIH document is seriously flawed for both failing to respect the standards of scientific discourse and failing to provide credible evidence to support its fundamental claims.

Science is normally advanced through publications that:

are signed by its authors;

include a comprehensive list of citations;

include contact information for at least one author;

are modifiable only through additional publications (including errata);

are open to rebuttal through published letters in the same journal;

are peer reviewed;

rely largely upon other peer-reviewed literature to back up their assumptions.

The NIAID web page has none of these characteristics. On the contrary:

it is anonymous;

citations are restricted to the protagonist case;

it changes occasionally without warning or explanation;

it has no forum for those who disagree with parts of it to respond;

it gives no information about the review process, if any, used to validate it;

prejudges the issue by labelling the dissident case as "myth" and the protagonist case as "fact";

fails to detail the dissident case in the same details as the protagonist case.

This rebuttal limits itself to revealing the fallacy of the key assertions made in the NIAID/NIH document:

(A) that "HIV fulfills Koch's postulates as the cause of AIDS";

(B) that "modern culture techniques have allowed the isolation of HIV in virtually all AIDS patients, as well as in almost all HIV-seropositive individuals" and that a human immunodeficiency virus (HIV) has been clearly identified;

(C) that so-called HIV antibody tests, when positive, indicate specific "antibodies that indicate HIV infection." That is, such antibodies are caused by HIV infection and nothing else.

Here we present evidence that all the various "HIV tests" (antibody, antigen, PCR (viral load) or by "modern culture techniques") have never been validated by the only possible standard of viral purification, nor has a unique AIDS-causing retrovirus ever been properly identified. Without the unequivocal gold standard of viral purification all the correlations put forward in the NIAID/NIH document as evidence that HIV causes AIDS have no solid foundation.

A point of clarification: This rebuttal draws largely on two major critics of the HIV/AIDS hypothesis: Papadopulos-Eleopulos et al. (known as the "Perth Group") and Peter Duesberg. On one essential point they hold fundamentally opposing views; Peter Duesberg accepts the isolation of HIV and the antibody tests as proof of infection (albeit with a harmless passenger virus) while the Perth Group does not. Readers might like to read The Last Debate (1999) which the Perth Group wrote to compare and contrast their views to those of Peter Duesberg. You can find Duesberg's defence of his position here.

A/ CLAIMS THAT KOCH’S POSTULATES HAVE BEEN FULFILLED

NIAID: “HIV fulfills Koch’s postulates as the cause of AIDS.”

The following is a short summary showing how HIV fails Koch's Postulates:

EPIDEMIOLOGICAL ASSOCIATION: Koch's Postulate #1. The microorganism must be found in all cases of the disease (NIAID/NIH).

NIAID: "…virtually all AIDS patients are HIV-seropositive; that is they carry antibodies that indicate HIV infection."

The assumption that a positive "HIV antibody" test indicates active HIV infection in every case is not supported by the scientific evidence. Also, the supposed correlation between a positive HIV antibody test and AIDS is extremely weak, based on circular logic and has been flawed from the very beginning.

On April 23, 1984 Dr. Robert Gallo filed a patent application for an antibody test, now generally referred to as the "AIDS test". The same day Gallo announced at an international press conference that he had discovered a new retrovirus that he called HTLV-III (now known as HIV), and that it was "the probable cause of AIDS". This announcement caught even the scientists in the audience by surprise. Gallo had circumvented an essential part of the scientific process; he had not published his research findings in any scientific or medical journal or subjected them to the normal process of peer review prior to being announced to the public.

When Gallo's "evidence" was finally published weeks later there were some serious problems. The laboratory procedure Gallo and his colleagues considered to prove isolation was positive in only 36% of his AIDS patients and only 88% were positive on the "HIV-antibody" test. Also, in order to ensure that only the AIDS patients and not the healthy control group came up positive on his antibody test, he had to dilute the blood an extraordinary 500-fold. At lesser dilutions too many healthy controls would also test positive. These facts alone should have been enough to cast serious doubt on Gallo's claim that he had discovered a new retrovirus or the "probable cause of AIDS" (Gallo, 1984; Papadopulos-Eleopulos, 1993a; Koliadin, 1998). An excellent summary of how corrupt, deceitful (and possibly even criminal) his research was can be found in the book Science Fictions by John Crewdson, a Chicago Tribune science writer (Crewdson, 2002)

There are tens of thousands of people who have been reported with AIDS to the CDC's HIV/AIDS Surveillance "without laboratory evidence regarding HIV infection":

Upon request, the CDC's director of the HIV/AIDS division, Harold Jaffe, stated that the HIV status of 43,606 out of the 253,448 American AIDS cases recorded by the end of 1992 was "not tested" (per. com., 1993). However this figure seems to be an understatement. Obviously, all 10,360 American AIDS cases diagnosed before the HIV antibody test, i.e., before 1985, were not tested (HIV/AIDS Surveillance, February 1993). In addition, the CDC published that "Approximately one third of AIDS patients in the United States have been from New York and San Francisco, where, since 1985, 7% have been reported with HIV-antibody test results, compared with 60% in other areas" (Confronting AIDS-Update 1988). Thus, between 1985 and 1987, 58% (93% x 1/3 + 40% x 2/3) of the 56,807 AIDS cases recorded in that period, or 32,948, have not been tested. For 1988, the CDC reported that 27% or 9,039 of the 33,480 AIDS cases recorded for that year were not tested for HIV (Selik, R. M., et al., 1990, J. AIDS 3, 73-82). According to the CDC's Technical Information Activity, 3682 AIDS cases without an HIV-test were recorded in 1989, 2888 in 1990, 1960 in 1991, and 1395 in 1992 (per. com., 1993). Thus, at least 62,272, or 18,666 more than Jaffe reports, were not tested (Duesberg, 1993).

There are thousands of people who have been diagnosed with AIDS even though they were found to be HIV negative on the antibody tests:

Determination of the HIV-AIDS correlation is further obscured because HIV-free AIDS cases are not recorded in the CDC's HIV/AIDS Surveillance. By 1993, at least 4621 HIV-free AIDS cases had been documented in the U.S., Europe, and Africa with the clinical AIDS definition . […] Some of these proved to be HIV-free even by PCR amplification of viral RNA and DNA (Duesberg, 1993).

In addition, HIV antibody tests are rarely used in Africa and other poor nations where the majority of people with AIDS supposedly reside, so there is no way of knowing how many test positive on the HIV antibody tests. In these parts of the world AIDS case definitions like the Abidjan/WHO, Bangui/WHO (clinical), Caracas/PAHO and revised Caracas/PAHO leave the door wide open for AIDS surveillance "without laboratory evidence regarding HIV infection". Surveys indicate that more than half of Africans who qualify for an AIDS diagnosis test HIV-negative:

227 patients with "AIDS": 59% test HIV-negative (Hishida, 1992)

122 patients with "AIDS": 69% test HIV-negative (Brindle, 1993)

913 patients with "AIDS": 71% test HIV-negative (Songok, 1994)

Finally, since positive HIV tests are now required in most wealthy nations to diagnose AIDS, even people suffering from one of the 29 "AIDS indicator diseases", with symptoms exactly like those of AIDS, are not diagnosed with AIDS if they have a negative "HIV antibody" test. This creates a ridiculous artificial correlation in which the definition of AIDS requires an HIV positive test, and then the artificial correlation is used to try to show that HIV must be causing AIDS. (Note: Under a few exceptional circumstances the CDC does not require proof of HIV infection e.g.; PCP pneumonia with no other apparent cause.)

In summary: If HIV antibody positive = HIV infection, clearly HIV is not found in all cases; and the definition also allows HIV to be absent. so HIV fails Koch's Postulate #1.


ISOLATION: Koch's Postulate #2. The pathogen must be isolated from the host and grown in pure culture (NIAID).

NIAID: "modern culture techniques have allowed the isolation of HIV in virtually all AIDS patients, as well as in almost all HIV-seropositive individuals..."

HIV has never been "isolated from the host and grown in pure culture." Proof of purification requires an electronmicrograph showing [pure] viral particles with the morphology of retroviruses -- and nothing else. Such an electronmicrograph has never been provided for HIV (Papadopulos, 1998b). Attempts to show the purity of so-called HIV isolates have been a complete failure (Gluschankof, 1997; Bess, 1997; De Harven, 1998a). Even Luc Montagnier, regarded as the discoverer of HIV, has admitted that his research team failed to purify a virus. He also said "analysis of the proteins of the virus demands mass production and purification. It is necessary to do that". His team "had not enough particles produced to purify and characterize the viral proteins" (Tahi, 1997). Since viruses and cells are made of proteins and nucleic acids, and especially since there are thousands of proteins and nucleic acids in cells, even if HIV did exist how is it possible to tell which constituents are viral and which are cellular? Attempts to show the purity of so-called HIV isolates have been a complete failure (Gluschankof, 1997; Bess, 1997; De Harven, 1998a). Even Luc Montagnier, regarded as the discoverer of HIV, has admitted that his research team failed to purify a virus. His team "had not enough particles produced to purify and characterize the viral proteins".

The word 'isolation' is commonly used in HIV research papers and, to most people, implies that the virus has been purified. Yet, in reality, the term has been degraded to utter meaninglessness because all that is looked for are surrogate markers (e.g. certain enzymes or proteins) which are believed to come from HIV. Not even one single intact viral particle is identified, and none of the surrogate markers that are used are actually specific to HIV (Eleopulos-Papadopulos et al, 1993). The process starts with unpurified extracts of body fluids being added to a culture of cancerous cells along with some stimulating chemicals. After several days or weeks, the culture is usually examined for one of the following signs: the reverse-transcriptase enzyme, the protein 'p24', retrovirus-like particles or proteins that bind with antibodies from AIDS patients. None of these are specific to retroviruses. Cultures are radically changed by being exposed to atmospheric oxygen levels (21%) rather than the 0.5-10% found within the body. It seems that this is just another indication that culture systems are unrepresentative of the real world: Roy S et al. Oxygen sensing by primary cardiac fibroblasts a k key role of p24. Circ Res. 2003; 92. ( Ranki, 1988; Roy; Papadopulos, 1993a).

See: Appendix A: The Origin of the "HIV" Proteins

The assumption that HIV can be isolated from "virtually all AIDS patients, as well as in almost all HIV-seropositive individuals" will be discussed in greater detail in sections B and C.

* See: What "HIV" Researchers Mean by "Isolation" and "Cloning"




The first electronmicrographs (EMs) of "purified HIV", published in the March 1997 issue of Virology, disclose "major contaminants". In the example above, note that the arrows labeled 'V' point to the few particles that are "retrovirus-like". The authors of these studies concede that their pictures reveal the vast majority of the material in the density gradient is cellular contamination (Bess el al, 1997). These particles can be dismissed straightaway because of their size; 234nm - over twice the diameter of any known retroviral particle.




By contrast, this electronmicrograph of the Friend virus shows, at a magnification of 19500 x, an almost pure population of typical "type C" viruses (not yet called retrovirus in 1965). The arrows point at contaminating debris and microvesicles. The interpretation was that virus purification was satisfactory and that contamination rate was extremely low and proves that retroviral particles can be purified (De Harven, 1965).


Figure 1.

TRANSMISSION PATHOGENESIS: Koch's Postulate #3. It must reproduce the original disease when introduced into a susceptible host (NIAID).

NIAID: "Postulate #3 has been fulfilled in tragic incidents involving three laboratory workers with no other risk factors who have developed AIDS or severe immunosuppression after accidental exposure to concentrated, cloned HIV in the laboratory."

Of the three people who supposedly got AIDS from 'purified' or 'concentrated' virus, only one has been discussed in any credible detail in the scientific journals. Duesberg is puzzled why these cases have not been written up in medical journals, as this would have been an opportunity to show that one of Koch's postulates of causation by a microbe has been fulfilled (Presidential AIDS Advisory Panel). There have been no scientific papers written about two of these three people and there have never been any further reports, even though these situations must have occurred no later than 1993 and since then millions of needlestick injuries have occurred.

NIAID: "In all three cases, HIV was isolated from the infected individual, sequenced and shown to be the infecting strain of virus."

Weiss et al report:

In a prospective cohort study of 265 laboratory and affiliated workers, one individual with no recognized risk factors for human immunodeficiency virus type 1 (HIV-1) infection was HIV-1 seropositive at the time of entry into the study. Molecular analyses of two HIV-1 isolates derived in two independent laboratories from a blood sample from this worker showed that the isolates were indistinguishable from a genotypic form of HIV-1 present in the H9/HTLV-IIIB cell line (Weiss. Science 1988, 239(4835):68-71).

This sounds impressive, but what does Weiss mean when he claims "the isolates were indistinguishable"? Valendar Turner offers a good analogy:

To speak of HIV DNA (i.e.; "molecular analyses") first one needs to prove that a particular sequence is unique and is present (as the RNA equivalent) in Retroviral-like particles proven to be a retrovirus (they aren't a virus until you prove they and they alone are what induce the appearance of more such particles). To proceed without such proof is no different from conducting a paternity suit where there is no proof that the DNA of the alleged father has been taken from the defendant or even a man. What defines the alleged father's DNA is solely that it comes from his body. It's no different with retroviruses. The operative expression is virologica habeas corpus. Amplification, sequencing, hybridization is wondrous stuff and keeps masses of scientists employed but their work is utterly meaningless in terms of a retrovirus if you don't have proof that's where it comes from.

To see the basic fallacy underlying these molecular analyses, consider the results of attempts at HIV isolation from a cell line like H9/HTLV-IIIB. Two papers in the leading science journal Virology in March 1997 provide astonishing data on the purification and isolation of HIV (Gluschankof et al, 1997; Bess et al, 1997). For the first time in the history of AIDS, elusive electron microscope images of 'HIV' collected or 'banded' at the official density required for purifying retroviruses, 1.16 gm/ml, were published. The electronmicrographs (EMs) disclosed "major contaminants" in "pure HIV" — an oxymoron to say the least. The authors of these studies conceded that their pictures reveal the vast majority of the material in the density gradient was cellular contamination. HIV expert Hans Gelderblom, of Berlin's Robert Koch Institute, co-authored the first paper which describes the contamination as "an excess of vesicles" - particles of cellular proteins, that may contain DNA or RNA. In a consecutive paper, a U.S. research team from the AIDS Vaccine Programme in Maryland reveal carefully, "It is unknown how these cellular proteins associate with the virus" and warn, "The presence of microvesicles in purified retroviruses has practical implications". One has to wonder how it could be possible to sequence an "HIV" genome or obtain pure HIV proteins from "isolates" like these. (See Figure 1.)

Eleopulos and colleagues summarize the problem:

The "HIV RNA" and "HIV DNA" are defined on the basis of length (approximately 10,000 nucleotides) and chemical composition (adenine rich) of all the RNA present in cultures of tissues of AIDS patients, NOT on the basis of RNA extracted from a particle first isolated and then proven to be a retrovirus.

In 1990 the HIV genome was said to consist of ten genes. This year Montagnier reported that HIV possesses eight genes and according to Barré-Sinoussi, HIV has nine genes. Neither is there constancy of the number of nucleotides in the "HIV genome". Also, to date, only 11 full length "HIV genomes" have been sequenced and accordingly, HIV genotype consignments are derived from sequence analysis of subgenomes measuring 2% to 30% of the total. The data is that such "genomes" vary between 3-40%. (If 30% of the HIV genome varies as much as 40%, how much does 100% of the HIV genome vary? In the HIV Western blot, how can an HIV producing one set of proteins detect antibodies that are produced in response to the set of all other disparate "HIV genomes"? When does "HIV" become some other entity?). Thus, not only are there no two HIV genomes of the same length or nucleotide composition, there is no single genetic entity "HIV DNA" to describe the myriads of "HIV genomes". It is also estimated that patients contain between one and one hundred million distinct HIV DNAs at the one time. Neither is it correct to encompass such DNAs under the umbrella of a quasispecies of "closely related genomes". (Papadopulos-Eleopulos, 1996).

NIAID: "In another tragic incident, transmission of HIV from a Florida dentist to six patients has been documented by genetic analyses of virus isolated from both the dentist and the patients."

Duesberg summarizes some of the evidence disproving the allegations against Dr. Acer:

Based on their own research, insurance companies concluded that the HIV strains in the five patients were different from that in Acer, meaning each caught it from a different source. (116) A study out of Florida State University has backed this conclusion. (117) Even the CDC acknowledged this evidence, though it still preferred to believe the dentist had infected Bergalis. But the CDC's own numbers give away the reality. An estimated 1 million Americans have HIV, in a total population of 250 million. Thus, 1 in 250 Americans have the virus. Five HIV-infected patients of Dr. Acer, out of 1,100 tested, comes to 1 in 220, virtually identical to the national average. [...] These HIV positive patients merely represent random samples from the general population.

The CDC's theory that AIDS was transmitted from Dr. Acer to his patient [Kimberly Bergalis] began to crumble in the mainstream press in 1994 when an investigative reporter researched the alleged victims of Dr. Acer. "He found weak evidence, shoddy science, and the work of a very accomplished malpractice attorney." (118)

The report first casts doubt on the time course of AIDS transmission from Dr. Acer to his patients. "[Bergalis] developed AIDS just two years after the surgery, and only 1 percent of HIV positive patients develop the full-blown disease that quickly." (119) The investigation disclosed that one of the six other patients that Acer presumably infected had visited the dentist's office only once for a cleaning by a hygienist, not by Acer himself. (120) The report further calls into question the exclusive reliance of the CDC and the malpractice attorney of the "Acer six" on the DNA fingerprinting technique to match Acer's virus with those of his patients. [...] Several experts have directly challenged the DNA fingerprinting that linked Acer to his patients, claiming that instead Bergalis's virus matched other HIV strains much more closely. (121) In view of this, a writer in the New York Times commented, "The CDC owes it to the public to reopen [Acer's] case." (122) (Duesberg, 1996)

Not one paramedic, emergency medical technician or surgeon in the U.S. has contracted AIDS from on-the-job exposure (CDC, 2000). Out of 733,374 total U.S. AIDS cases through 1999, only 25 are thought to be occupationally acquired, based on presumptive evidence — meaning they admitted no other risk factor (CDC, 2000). In Canada, out of 17,389 AIDS cases through 2000, only 5 are reported as occupationally acquired (PPHB, 2001). Only one case has been documented, and the evidence was weak and circumstantial (CCDR, 1992). Consider that the 1 million needle-stick injuries among health care workers in the U.S. each year result in about 1,000 cases of hepatitis among health care workers annually. That means that in the 18 years of AIDS, health care workers contracted 18,000 cases of hepatitis and 25 cases of AIDS. Pretty strange if HIV is a blood-borne virus!

B/ CLAIMS THAT HIV ISOLATION HAS BEEN ACHIEVED

NIAID: "HIV can be detected in virtually everyone with AIDS."

"Recently developed sensitive testing methods, including the polymerase chain reaction (PCR) and improved culture techniques, have enabled researchers to find HIV in patients with AIDS with few exceptions. HIV has been repeatedly isolated from the blood, semen and vaginal secretions of patients with AIDS, findings consistent with the epidemiologic data demonstrating AIDS transmission via sexual activity and contact with infected blood (Bartlett, 1999; Hammer et al. J Clin Microbiol 1993;31:2557; Jackson et al. J Clin Microbiol 1990;28:16)."

New testing techniques cannot both be validated against existing antibody tests and used to support current tests. They must, instead, be independently validated using the only technique that unambiguously detects HIV - virus purification.

In a letter to the editor of the British Medical Journal, Eleopulos et al simply states the problem and invites speculation as to how all those "extra" Africans become HIV positive:

EDITOR - According to Lamptey, in Africa slightly more than 80% of infections are acquired heterosexually.1 The high rates of heterosexual infection in Africa have been generated by actuarial models and antenatal data.2 These high rates are not supported by data originating from prospective epidemiological studies.

In 1997 Padian et al published the results of a 10 year study on heterosexual transmission of HIV in northern California.3 The data were divided into two parts, cross sectional and prospective. From the cross sectional study it was estimated that infectivity for male to female transmission is low, approximately 0.0009 per contact, and approximately eight times more efficient than female to male transmission. Using this estimate of male to female transmission, it would take 770 or 3333 sexual contacts respectively to reach a 50% or 95% probability of becoming infected. If sexual contact were to take place repeatedly every three days this would require a period of 6.3 and 27.4 years respectively. Based on the estimate of female to male transmission by Padian et al it would require 6200 and 27 000 contacts and a period of 51 and 222 years, respectively (table).

Numbers of years to attain 50% and 95% probability of transmission of HIV in United States and Uganda assuming sexual contact once every three days
Probability per contact No of years for 50% probability No of years for 95% probability
United States
Male to female 0.0009 6.3 27.4
Female to male 0.0001125 51 222
Uganda
Male to female 0.0009 6.3 27.4
Female to male 0.0013 4.4 19.5

In 2001 a community based study was reported from Uganda, where 174 monogamous couples, in which one partner was HIV-1 positive, were retrospectively identified from a population cohort involving 15 127 people.4 The probability of transmission per sexual contact was 0.0009 for male to female and 0.0013 for female to male respectively (table). The authors concluded that the probability of HIV transmission per sex act in Uganda is comparable to that in other populations, suggesting that infectivity of HIV subtypes cannot explain the explosive epidemic in Africa (R H Gray et al, eighth conference on retroviruses and opportunistic infections, Chicago 2001). In other words, there is no more heterosexual transmission of HIV in Africa than anywhere else, including Britain, the United States, Australia, and Europe. (Papadopulos-Eleopulos et al, 2002)

"Recent data has challenged the whole notion that the majority of HIV infections in Africa are heterosexual." (Brewer DD, 2003; Gisselquist D et al, 2002; Gisselquist D et al, 2003a; Gisselquist D et al. 2003b)

The statement quoted above from the NIAID document cites three references to support its claim that newer tests have allowed HIV to be 'repeatedly isolated' from people diagnosed with AIDS. When these three references are examined, however, one finds that they actually point out many inconsistencies and problems with the tests currently being used, and in some cases these uncertainties are openly admitted. This is a perfect example of the paucity of evidence and misleading references put forward by the NIAID/NIH in support of their claims. Following is a brief analysis of how the three references for the above NIAID/NIH statement are inadequate and misleading:

Bartlett, 1999; 2001-2002 Medical Management of HIV Infection by John G. Bartlett, M.D. and Joel E. Gallant, M.D., M.P.H. Copyright © 1997-2002 The Johns Hopkins University on behalf of its Division of Infectious Diseases and AIDS Service. "Production of the 2001-2002 edition of Medical Management of HIV Infection has been underwritten by an unrestricted educational grant form GlaxoSmithKline, Inc."

The relevant section reads as follows:

Viral Detection: Other methods to establish HIV infection include techniques to detect HIV antigen, DNA, or RNA (Table 2-1). HIV-1 DNA PCR is the most sensitive and can detect 1-10 copies of HIV proviral DNA. None of these tests is considered superior to routine serology in terms of accuracy, but some may be useful in patients with confusing serologic test results, when there is a need to clarify indeterminate test results, for virologic monitoring in therapeutic trials, and for HIV detection when routine serologic tests are likely to be misleading such as in patients with agammaglobulinemia, acute retroviral infection, neonatal HIV infection, and patients in the window following viral exposure. In most cases, confirmation of positive serology is accomplished simply by repeat serology. The sensitivity of tests for detection of HIV varies with the stage of disease and test technique, but is usually reported at >99% for DNA-PCR, 90% to 95% for quantitative HIV-RNA, 95% to 100% for viral culture of peripheral blood mononuclear cells (PBMC), and 8% to 32% for p24 antigen detection (J Clin Microbiol 1993;31:2557; N Engl J Med 1989;321:1621; J AIDS 1990;3:1059; J Infect Dis 1994;170:553; Ann Intern Med 1996;124:803). None of these tests should replace serology to circumvent the informed consent process.

None of this sounds like evidence that there are valid tests for detecting HIV that could be considered a gold standard for "routine serology", that is, HIV antibody tests. It is clear that antibody tests do not prove presence of a virus. DNA, RNA and protein antigens are contingent upon proof they are extracted from pure culture of virus.

A foot note at the bottom of the page of the internet version of this publication states: "Physicians and other health care professionals are encouraged to consult other sources and confirm the information contained in this site ...." So perhaps we had best move on.

Hammer et al. J Clin Microbiol 1993;31:2557. Use of virologic assays for detection of human immunodeficiency virus in clinical trials: recommendations of the AIDS Clinical Trials Group Virology Committee.

This is a set of guidelines or tutorial similar to the Medical Management of HIV Infection. Rather than providing evidence that "HIV can be detected in virtually everyone with AIDS", it strongly suggests the opposite. In the section on Viral Isolation two assays are discussed; PBMC culture and plasma culture. Regarding the PBMC culture:

(iv) Indicated use: diagnosis. For a specimen to be considered positive by either the quantitative microculture assay or the qualitative macroculture assay, the sample supernatant must contain 30 pg or more of p24 antigen per ml, as determined by the standard p24 EIA. This arbitrary positive value has been determined historically on the basis of average positive values from various kit manufacturers and is unrelated to that used for determining positivity in sera or plasma.

In the following discussion of plasma culture Hammer et al. state:

Plasma viremia is not apparent in all HIV-positive patients. Infectious virus is rarely detectable in patients with CD4+ cell counts above 500/mm3. As the CD4+ cell count drops, the percentage of patients with detectable plasma viremia will increase. For practical purposes, plasma viremia cultures should only be attempted when CD4+ counts are <200/mm3 and are accompanied by a positive baseline cell culture.

See Table 1 in the Piatak paper to get some perspective on how much "plasma viremia will increase."(Piatak, 1993). Hammer et al. also suggest that a DNA PCR assay could be used for diagnosis, but with this qualification:

For the diagnosis of HIV-1 infection, two specimens collected at different times must be HIV-1 positive by PCR as defined above. There is still some question at this time regarding confirmation of the PCR positive results by culture.

Jackson et al. J Clin Microbiol 1990;28:16. Human immunodeficiency virus type 1 detected in all seropositive symptomatic and asymptomatic individuals.

This paper claims to 'isolate' HIV in 100% of people who had been previously diagnosed HIV-positive using the antibody tests, but there are a number of inconsistencies in its claims. The first major inconsistency is that the vast majority of similar studies have been able to 'isolate' HIV in much less than 100%, and even as low as 20%, of people diagnosed 'HIV-positive', so that using this study as a reference is misleading, at best. Another major inconsistency is that the word 'isolation' is used to describe the detection of surrogate markers which are not specific to HIV, as discussed above. Papadopulos-Eleopulos et al. provide a thorough refutation of this study's conclusions:

In their 1990 paper Jackson et al reported that "Between February 1987 and October 1988, peripheral blood mononuclear cells (PBMC) from 409 individuals who were antibody positive for HIV-1 by Western (immuno) blot (56 AIDS patients, 88 patients with ARC, and 265 asymptomatic individuals) were cultured". "Using a sensitive technique previously described", the p24 assay noted above, they reported that "HIV-1 can be isolated from 100% (56 of 56) of AIDS patients, 99% (87 of 88) of ARC patients, and 98% (259 of 265) HIV- 1 antibody positive asymptomatic individuals". Not one of "131 HIV- 1 antibody-negative individuals has a positive culture". Using the same p24 assay (Abbott) they tested the serum from 403 out of the 409 individuals. The test was positive in 23/56 (42%) AIDS patients, 31/88 (57%) ARC patients and 44/259 (17%) asymptomatic antibody positive individuals. For unstated reason(s) a positive serum test is considered proof for the detection of "HIV-1 antigen in serum" while the same positive culture test is considered proof for "HIV-1 isolation" from the culture. There are many reasons to question the interpretation of the p24 assay: (a) The p24 assay is an antibody/antigen reaction and is subject to ubiquitous background reactivity. In this context, even if "two serial supernatant samplings with the later sampling showing greater reactivity", even if double or triple, for example, 30 and 60 or 30 and 90, both readings may be nothing else but background readings. Jackson and colleagues' criteria are not even in agreement with those used by Ho et al which are equally as arbitrary […] Even without a gold standard [i.e.; HIV isolation], the non-specificity of the p24 antigen test is so obvious that it is accepted by no less an authority on HIV testing than Philip Mortimer and his colleagues from the UK Public Health Laboratory Service, "Experience has shown that neither HIV culture nor tests for p24 antigen are of much value in diagnostic testing. They may be insensitive and/or non-specific".(236) […] Jackson et al's claims are not even confirmed by other laboratories. According to Jackson et al, up until 1990 only three small studies reported "100% isolation rates of HIV-1 from AIDS patients". In all the other studies, "HIV-1 was not isolated from 6 to 50% of HIV-1 seropositive AIDS cases reported. The culture recovery rate of HIV-1 from HIV-1 antibody positive asymptomatic patients has generally been even lower, only 20 to 42% in some studies".(Papadopulos-Eleopulos, 1996)

An example of a study with typically low rates of viral 'isolation', was published by Piatak, et al.(1993). This study not only found that many people diagnosed HIV-positive using antibody tests had no 'culturable' virus, but also found that only 53% of people with measurable 'viral loads' had positive viral cultures. See Table 1 (Piatak, 1993).

Table 1. [detail] [full table]

"Plasma virus levels determined by QC-PCR correlated with, but exceeded by an average of 60,000-fold, virus titers measured by endpoint dilution culture." (Piatak et al.)


In the table above from Piatak et al.(1993) the column entitled "HIV RNA" shows the "viral loads" of the individual people listed, while the column entitled "Plasma culture/TCID" shows how much virus they could find using techniques claimed to "culture" the virus - note that most people with viral loads have no culturable virus, even with viral loads in the hundreds of thousands. One patient with CDC Stage IV AIDS had a viral load of 815,000 per ml of blood plasma even though he had no "culturable" virus (not shown in this detail of the table).

C/ CLAIMS THAT HIV ANTIBODY TESTS ARE VALID

NIAID: "Diagnosis of infection using antibody testing is one of the best-established concepts in medicine. […]. Current HIV antibody tests have sensitivity and specificity in excess of 98% and are therefore extremely reliable (WHO, 1998; Sloand et al. JAMA 1991;266:2861).

"Progress in testing methodology has also enabled detection of viral genetic material, antigens and the virus itself in body fluids and cells. While not widely used for routine testing due to high cost and requirements in laboratory equipment, these direct testing techniques have confirmed the validity of the antibody tests (Jackson et al. J Clin Microbiol 1990;28:16; Busch et al. NEJM 1991;325:1; Silvester et al. J Acquir Immune Defic Syndr Hum Retrovirol 1995;8:411; Urassa et al. J Clin Virol 1999;14:25; Nkengasong et al. AIDS 1999;13:109; Samdal et al. Clin Diagn Virol 1996;7:55."

As with the claim "HIV can be detected in virtually everyone with AIDS", the anonymous authors have provided spurious references that do not support their assertions. Seven of the eight references have nothing to do with attempting to confirm the validity of the antibody tests. Only the Jackson et al. reference can be considered appropriate, but their conclusions are based on the flawed logic discussed above. See previous discussion of Piatak et al.

Even if one were to accept the existence of a unique "HIV" retrovirus with an outer coat composed of unique proteins ('antigens'), this still does not prove that antibody tests are accurate. No antibody test can distinguish between HIV antibodies (if they exist) and cross-reacting non-HIV antibodies unless the specificity of the test is established by comparing the presence of antibody reactivity (a 'positive' test result) when virus purification is successful, and the absence of antibody reactivity when virus purification fails. No data in the scientific literature has reported this essential verification. HIV antibody tests are therefore not grounded in reality, and may be meaningless.

The same applies to "viral load" (PCR) tests:

If you have to use PCR to find something, that automatically means that what you find has no pathological relevance. Piatak, et al.(1993) were able to successfully "isolate" virus from only 53% of people with measurable viral loads. See Table 1 (Piatak, 1993). Thus the diagnosis "HIV-positive" is of questionable scientific value and needs to be reappraised.

Eleopulos el al remind us of this revealing meta-analysis of the sensitivity and specificity of PCR:

Researchers from several institutions in the USA performed a meta-analysis of studies published between 1988 and 1994 that evaluated the sensitivity and specificity of PCR (Owens DK, et al. 1996). They "accepted positive results on conventional antibody tests (if they included a confirmatory Western Blot analysis or similar test) or viral cultures as high-quality evidence of infection", that is, as a gold standard. In a search of 17 computer databases, they "identified 5698 titles of potentially relevant articles. After independent review by two readers, 1735 titles were judged to be potentially relevant". Then they "reviewed the associated abstracts and then selected 379 studies published as full articles for further review. Of these 379 articles, 96 met the inclusion criteria and were analyzed". They found that: "Measured performance was extremely variable. When indeterminate PCR results were excluded, sensitivity ranged from 10% to 100% and specificity from 0% to 100%". They concluded "Our investigation produced two main findings. First, the false-positive and false-negative rates of PCR that we determined are too high to warrant a broader role for PCR in either routine screening or in the confirmation of diagnosis of HIV infection. This conclusion is true even for the results reported from more recent, high-quality studies that used commercially available, standardized PCR assays...We did not find evidence that the performance of PCR improved over time" (Papadopulos-Eleopulos E, et al. 2001).

Why does there seem to be a correlation between so-called HIV antibodies and AIDS defining illness?

Without carefully controlled, unbiased studies to determine the clinical significance of HIV tests, it's hard to know what positive results may or may not indicate. It seems clear that people who fall into the AIDS risk groups and test positive on these antibody tests are more likely to develop the illnesses classified as AIDS - as well as diseases which are not classified as AIDS. The so-called AIDS diseases occur principally in people with a history of repeated exposure to foreign proteins and /or toxins: multiple STDs and other viral, bacterial and parasitic infections; various pathogens via injecting contaminated street drugs; recreational and pharmaceutical drugs; commercially-made clotting factor and blood transfusions. They may also occur in the chronically malnourished due to their weakened immune systems and subsequent exposure to more pathogens. These exposures to various pathogens, foreign proteins and toxins may elicit enough antibodies to register on the non-specific HIV antibody tests. Such a high level of antibody activity is not usually found among healthy people who are not in any AIDS risk group.

Papadopulos-Eleopulos points out that it is practically impossible to obtain clear data on this issue:

In other words, follow people with a positive test over a period of years and see who developed AIDS and who did not. The trouble is it would be very difficult for most people knowing they are HIV positive, as well as their physicians, not to believe that sooner or later they're going to get very sick and eventually die of AIDS. And that mindset may greatly effect the results of such an experiment. (Johnson, 1997)

The "modern culture techniques" and the various indirect markers that HIV researchers regard as the equivalent of HIV isolation were discussed in detail above. Here it is worth noting that Eleopulos et al. argue that the various markers thought to indicate HIV infection can only be detected when cultures derived from the patients' tissue are subjected to extreme biological and chemical stress. Known as oxidative stress, these conditions are comparable to what happens in our bodies when exposed to the long list of stressors described above. This kind of oxidative stress may cause the conditions that then cause the HIV test to react positive, as well as increasing the risk of a person developing AIDS-like illnesses (Papadopulos-Eleopulos. 1992; Giraldo RA.).

See: Appendix B: The correlation between "HIV" antibodies and AIDS diseases

There are no simple answers to the mystery of AIDS. The illnesses do exist, even though they probably do not have a single cause. The HIV antibody tests may not indicate the presence of a virus, but people who come down with AIDS-like diseases are more likely to test positive. It is likely that an association between the diseases and the antibodies is due to a number of health risk factors. In Western countries, the biggest factor in illness appears to have been drug use, whether injected, ingested or inhaled, with different patterns of use leading to different diseases. In Third World countries, malnutrition can lead to a wasting condition that meets the Bangui definition of AIDS. Antiviral drugs are highly toxic, and can also lead to many of the diseases defined as 'AIDS'. Addressing known health risks is often much safer, cheaper and more effective than placing millions of people on lifelong pharmaceutical therapy. (Duesberg, P, Rasnick, D.)

Many HIV antibody positive people - some diagnosed over 17 years ago - remain healthy without HIV drugs and have never developed AIDS. For many people, being diagnosed HIV positive may have no bearing on their probability of living a long, healthy life. Clearly, testing positive on such a non-specific test does not always mean that one is in danger of acquiring immune deficiency. On the other hand, the idea of "HIV positive" has taken on devastating significance in the popular consciousness. The patients' health - physical and psychological - may be seriously compromised by an "HIV positive" diagnosis. Their physicians may feel compelled to offer treatments, even in the absence of clinical symptoms, with drugs well documented for their toxic effects. To confound things further, many of the toxic effects are indistinguishable from symptoms of AIDS (DeSimone, 2000).

Alive and Well founder and spokesperson Christine Maggiore recently summarized her perception off the human toll of the failed HIV/AIDS hypothesis:

Whenever I speak in public someone invariably asks, "If HIV doesn't cause AIDS, why do a lot of people who test HIV positive get sick and die?" I think a better question is: How does anyone who tests positive remain well? Between the initial devastation of the diagnosis, the subsequent social isolation, dire predictions by doctors, lab tests measuring out our remaining time, medical care that assumes our inevitable early demise, AIDS organizations poised to usher us into death, negative expectations of friends, family and the public, constant media reports on the incurable fatal virus, pressure to consume toxic drugs, to regard ourselves as infected, abnormal, and ill, pitches to sell off our life insurance, exchange work for disability, and get a handicapped parking pass, and official orders to keep a safe, latex-covered distance from people we love, I wonder how so many of us manage to live.




Appendix A: The Origin of the "HIV" Proteins

Appendix B: The correlation between "HIV" antibodies and AIDS diseases


Review Papers in the Medical Journals

Papadopulos-Eleopulos et al.

Is a Positive Western Blot Proof of HIV Infection? Bio/Technology Vol. 11 June 1993.

Has Gallo Proven the Role of HIV in AIDS? Emergency Medicine 1993;5:5-147.

AIDS in Africa: Distinguishing Fact and Fiction. World Journal of Microbiology & Biotechnology (1995) 11, 135-143.

HIV Antibodies: Further Questions and a Plea for Clarification. Current Medical Research and Opinion Vol. 13: 627-634, 1997.

HIV Antibody Tests and Viral Load — More Unanswered Questions and a Further Plea for Clarification. Current Medical Research and Opinion Vol. 14: 185-186, 1998.

Etienne de Harven

Viral Etiology of Human Cancer: A historical perspective. Haematologica Journal of Hematology volume 84 - number 5 - May 1999

Peter Duesberg

Human Immunodeficiency virus and acquired immunodeficiency syndrome: Correlation but not causation. Proc. Natl. Acad. Sci. USA Vol.86, pp. 755-764, 1989

AIDS epidemiology: Inconsistencies with human immunodeficiency virus and with infectious disease. Proc. Natl. Acad. Sci. USA Vol. 88, pp. 1575-1579, 1991

Peter Duesberg & Jody R. Schwartz

Latent Viruses and Mutated Oncogenes: No Evidence for Pathogenicity. Progress in Nucleic Acid Research and Molecular Biology 43:135-204, 1992

Peter Duesberg & David Rasnick

The AIDS dilemma: drug diseases blamed on a passenger virus. (pdf version) Genetica 104: 85-132, 1998


Acknowledgments

We thank Eleni Papadopulos-Eleopulos and Valendar Turner at the Royal Perth Hospital, University of Western Australia for their tireless work and generosity. We would also like to thank Peter Duesberg and David Rasnick, who have made many sacrifices challenging the ruthlessly guarded HIV=AIDS hypothesis.



For our critique of another notorious document see the Durban Declaration Rebuttal. The "Durban Declaration" was published in Nature on July 6 2000, and our rebuttal was written a few months later and is available online at http://thedurbandeclaration.org.



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Study Charts Risk of Heterosexual HIV Transmission is rare -- even rarer with condoms

San Francisco Chronicle - The Voice of the West, 901 Mission Street, San Francisco, CA 94119 - Tuesday, August 26, 1997 - Page A2
Chronicle Staff Report
Infection by the AIDS virus through heterosexual transmission is extremely rare in the United States, but there are clear dangers, according to the most detailed study of its kind ever done.

Anal sex, failure to use condoms, injection drug use and the presence of a sexually transmitted disease are the strongest predictors of AIDS infection, the study found.

Dr. Nancy Padian, an AIDS researcher at the University of California in San Francisco, and her colleagues have just completed the nation's most extensive study of risk factors in AIDS transmission among heterosexual couples. They found infections of women by men occurred in only 9 of every 10,000 sexual encounters. And even that low rate was eight times higher than it was for men infected by women, the Padian study showed. The study, published in this month's issue of the American Journal of Epidemiology, followed 82 HIV-infected women and their male partners, as well as 360 HIV-infected men and their female partners for 10 years.

The volunteers for the study were interviewed and given physical exams every six months and also counseled during each visit about safe sexual practices.

The researchers said they observed dramatic behavior changes during the study. For example, when the study began, no couple was abstaining from sex, only 32.2 percent ever used a condom and 37.9 percent were having anal sex. By the final follow-up visit 10 years later, 14.5 percent said they abstained from sex, 74 percent used condoms and only 8.1 percent had anal sex. "We now know many of the risk factors that affect the likelihood of transmission between uninfected individuals and their heterosexual partners," Padian said. "Elimination or modification of these factors would result in reduced transmission of HIV."