Free Crack Pipes Urged To Slow Spread Of HIV In SF, Leaders Balk At Idea

SAN FRANCISCO (KPIX 5) – Brows were raised and eyes rolled back when needle exchange programs were first implemented to stop the spread of disease. Giving away free and clean syringes to heroin users seemed preposterous to many. Now it is a common practice and almost universally accepted as a means to prevent the spread of HIV. Could the same happen with free crack pipes?

Soon after our story was posted Friday, KPIX 5 received a flurry of phone calls and emails from city officials denouncing the idea to distribute the crack pipes.

Mayor Ed Lee was first with a statement, via an email from his spokesperson, Christine Falvey: “Mayor Lee is not aware of this exploration and is not supportive. There are many other HIV interventions that could and should be explored before ever considering this.”

1983 AIDS had become big enough in the American and European press to pique the interest of the influential infectious disease establishment, particularly the cancer virus hunters.

At that time the virus hunters had been engaged for over a decade in president NixonÂ’s War on Cancer with unsuccessful attempts to find a human cancer virus (Duesberg 1996b; Fujimura 1996; de Harven 1999).

Now they were looking for new diseases that could be attributed to viruses (Duesberg 1987). Perhaps AIDS could at last yield clinically relevant lymphoma-, KaposiÂ’s sar- coma- or immunodeficiency-viruses (Duesberg 1996b). Indeed, virus hunters from the CDC were the first to alert the public that AIDS may be Â“transmissibleÂ” (Francis et al 1983).

A similar alert came from a French virus team, which had discovered a retrovirus in a homosexual man at risk for AIDS, which a year later became the accepted cause of AIDS (Barre-Sinoussi et al 1983).

News, that the cause of AIDS may be a virus, and thus transmissible to the general population, immediately set off a national panic that opened the doors for new surveillance programs by the CDC and predictably set off a race among virus hunters for the AIDS virus (Shilts 1987).

According to an international press conference called by the US Secretary of Health and Human Services in Washington DC on 23 April 1984, that race was won by government researchers from the NIH who had found in some AIDS patients antibodies against a new retrovirus closely related to a hypothetical human leukemia virus (Altman 1984).

The virus was introduced as fortunate fallout of the failed War on Cancer. The next day the new virus was already termed, the Â“AIDS virusÂ”, by the New York Times (Altman 1984). Overnight nearly all AIDS researchers dropped the lifestyle-AIDS hypothesis to work on the new Â“AIDS virusÂ”, which was already endorsed by the US government.

The CDCÂ’s director of the Task retrovirologists officially sealed the seemingly tight package of a new Â“AIDS virusÂ” and the CDCÂ’s assumption that immunodeficiency was the common denominator of the 26 AIDS-defining diseases (table 1) by naming it, Human Immunodeficiency Virus (HIV) (Coffin et al 1986).

Even before the AIDS virus became the officially accep- ted cause of AIDS, the CDC had already made antibodies against the virus the only definitive criterion to diagnose any of the heterogeneous diseases as AIDS in 1985 (Cen- ters for Disease Control 1985, 1987, 1992).

Their unortho- dox decision to use antibodies against the virus (normally functioning as a vaccine), instead of the virus, for the diagnosis of AIDS was based on the flawed analogy with some bacterial pathogens. For example, syphilis bacteria can be pathogenic despite the presence of antibodies, e.g. the Wassermann test for syphilis (Brandt 1988).

But viruses are typically unable to enter cells in the presence of anti-viral antibodies Â– the basis for the effectiveness of Jennerian vaccines. Because of the CDCÂ’s decision, AIDS is diagnosed worldwide if antibody against (!) HIV, rather than HIV, is detectable in a patient along with any of the CDCÂ’s 26 diseases.

Since 1992 even low T-cell counts are diagnosed as a condition, termed Â“HIV/AIDSÂ”, which is treatable with anti-HIV drugs provided it occurs in the presence of antibodies against HIV (Centers for Disease Control 1992), (see table 1, and Â§ 4.2). 3.1 Discrepancies between the predictions of the virus-AIDS hypothesis and the facts.

Despite its spectacular birthday the HIV-AIDS hypothesis has remained entirely unproductive to this date: There is as yet no anti-HIV-AIDS vaccine, no effective prevention and not a single AIDS patient has ever been cured Â– the hallmarks of a flawed hypothesis. Indeed the hypothesis was born with several serious birth defects and has developed further defects since; most of these should have given pause to HIV-AIDS researchers to rethink and reconsider.

However, in the race to claim a share of the new viral cause for AIDS and of virus-based AIDS treat- ments, Â“The Trojan horse of emergencyÂ” (Szasz 2001) was saddled so quickly that there was little time and no interest to address these defects, not even the most fundamental ones (Weiss and Jaffe 1990; Cohen 1994; OÂ’Brien 1997).

An analysis of the defects of the HIV-AIDS hypothesis based on its failure to predict AIDS facts is shown in table 4. Our analysis is based on the most recent and most authoritative case made for the HIV-AIDS hypothesis since 1984, namely the Durban Declaration that was published in Nature in 2000 and has been signed by Â“over 5,000 people, including Nobel prizewinnersÂ” (The Durban Declaration 2000). It can be seen in table 4 that the HIV-hypothesis fails to predict 17 specific facts of AIDS.

The most fundamental discrepancy between the HIV-AIDS hypothesis and the facts is the paradox, that a latent, non-cytopathic and immunologically neutralized retrovirus [a virus that is inherently not cytopathic (Duesberg 1987)], that is only present in less than 1 out of 500 susceptible T-cells and rarely expressed in a few of those, would cause a plethora of fatal diseases in sexually active, young men and women.

And, that the plethora of the diseases attributed to this virus would not show up for 5Â–10 years after infection (table 4). As a result of the many discrepancies between the HIV hypothesis and the facts, we conclude that HIV is not sufficient for AIDS, and is most compatible with being a passenger virus. Surprisingly our conclusion is supported by a survey of AIDS researchers conducted by the New York Times, shortly after the publication of the Durban Declaration.

At the 20th anniversary of AIDS, on 30 January 2001, the New York Times interviewed a dozen leading AIDS researchers for an article that turned into a list of questions, Â“The AIDS questions that lingerÂ” (Altman 2001a), similar to those asked by us in table 4: Â“In the 20 years since the first cases of AIDS were detected, scientists say they have learned more about this viral disease than any other, and few have dispu- ted the claim. Â… Despite the gains Â… experts say reviewing unanswered questions could prove useful as a measure of progress for AIDS and other diseases.

Such a list could fill a newspaper, and even then would create debate. (E.g.): How does H.I.V. subvert the immune system? . . . Why does AIDS predispose infec- ted persons to certain types of cancer and infections and not others? . . . Dr Anthony S Fauci, the director of the National Institute of Allergy and Infectious Diseases, said, Â‘It is the rare person who gets up and strips himself of his personal agenda and articulates what we really do not know because by saying that they would diminish the impact of their own work, which is their agendaÂ’.

(Regarding anti-HIV medications:) . . . the new drugs do not completely eliminate H.I.V. from the body, so the medicines, which can have dangerous side effects, will have to be taken for a lifetime and perhaps changed to combat resistance.

The treatments are now so complicated that it is difficult, expensive and time-consuming to answer basic and practical questions. What combinations of drugs should be started first and when? Why do side effects like unusual accumulations of fat in the abdomen and neck develop? . . . Anti-H.I.V. drugs suppress replication of the virus, which should give the functioning parts of the immune system a chance to eliminate re- maining virus.

That does not happen. Â‘So something is bizarre about that, that we donÂ’t understandÂ’, Dr Fauci said. Is a vaccine possible? . . . many unanswered questions exist about whether and when one can be developed.Â” Thus HIV-AIDS researchers have not solved the discrepancies and paradoxes of the HIV-AIDS hypothesis, but still do not follow the scientific method of searching for alternative explanations (Costello 1995).

Since 19 years of HIV-AIDS research have failed to produce tangible benefits for AIDS patients and risk groups, and since there are no paradoxes in nature only flawed hypotheses, the scientific method calls for an alternative, testable hypothesis. Here we offer one such hypothesis.

Our hypothesis extends the early, and now abandoned Â“lifestyleÂ” hypothesis (Â§ 2) and subsequent drug-AIDS hypotheses from us and others (Duesberg 1992; Duesberg and Rasnick 1998). Â“Historically, the first step in determining the cause of any disease has always been to find out if there is anything, apart from the disease itself, that sufferers have in commonÂ” (Cairns 1978).

However, the traditional search for the cause is only completed, if something that suf- ferers have in common can also be shown to cause the disease; in other words if KochÂ’s postulates can be ful- filled (Merriam-Webster 1965). This is true for viruses just as much as for drugs. Following this tradition, we try here to provide proof of principle for our drug and malnutrition hypothesis of AIDS Â– alias chemical AIDS. 4.1

The chemical-AIDS hypothesis and its predictions The chemical-AIDS hypothesis proposes that the AIDS epidemics of the US and Europe are caused by recreational drugs, alias lifestyle, and anti-HIV drugs (Duesberg.

1. Since HIV is Â“the sole cause of AIDSÂ”, it must be abundant in AIDS patients based on Â“exactly the same criteria as for other viral diseases.Â” But, only antibodies against HIV are found in most patients (1Â–7)**. Therefore, Â“HIV infection is identified in blood by detecting antibodies, gene sequences, or viral isolation.Â”

But, HIV can only be Â“isolatedÂ” from rare, la- tently infected lymphocytes that have been cultured for weeks in vitro Â– away from the antibodies of the human host (8). Thus HIV behaves like a latent passenger virus.

2. Since HIV is Â“the sole cause of AIDSÂ”, there is no AIDS in HIV-free people.

But, the AIDS literature has described at least 4621 HIV- free AIDS cases according to one survey Â– irrespective of, or in agreement with allowances made by the CDC for HIV-free AIDS cases (55).

3. The retrovirus HIV causes immunodeficiency by killing T-cells (1Â–3).

But, retroviruses do not kill cells because they depend on viable cells for the replication of their RNA from viral DNA integrated into cellular DNA (4, 25). Thus, T-cells infected in vitro thrive, and those patented to mass-produce HIV for the detection of HIV antibodies and diag- nosis of AIDS are immortal (9Â–15)!

4. Following Â“exactly the same criteria as for other viral disea- sesÂ”, HIV causes AIDS by killing more T-cells than the body can replace. Thus T-cells or Â“CD4 lymphocytes . . . become depleted in people with AIDSÂ”. But, even in patients dying from AIDS less than 1 in 500 of the T-cells Â“that become depletedÂ” are ever infected by HIV (16Â–20, 54). This rate of infection is the hallmark of a latent passenger virus (21). 5. With an RNA of 9 kilobases, just like polio virus, HIV should be able to cause one specific disease, or no disease if it is a passenger (22).

But, HIV is said to be Â“the sole cause of AIDSÂ”, or of 26 different immunodeficiency and non-immunodeficiency diseases, all of which also occur without HIV (table 2). Thus there is not one HIV-specific disease, which is the definition of a passenger virus!

6. All viruses are most pathogenic prior to anti-viral immunity. Therefore, preemptive immunization with Jennerian vaccines is used to protect against all viral diseases since 1798.

But, AIDS is observed Â– by definition Â– only after anti- HIV immunity is established, a positive HIV/AIDS test (23). Thus HIV cannot cause AIDS by Â“the same criteriaÂ” as conventional viruses.

7. HIV needs Â“5Â–10 yearsÂ” from establishing antiviral immu- nity to cause AIDS.

But, HIV replicates in 1 day, generating over 100 new HIVs per cell (24, 25). Accordingly, HIV is immunogenic, i.e. biochemically most active, within weeks after infection (26, 27). Thus, based on conventional criteria Â“for other viral disea- sesÂ”, HIV should also cause AIDS within weeks Â– if it could.

8. Â“Most people with HIV infection show signs of AIDS within 5Â–10 yearsÂ” Â– the justification for prophylaxis of AIDS with the DNA chain terminator AZT (Â§ 4).

But, of Â“34â‹…3 million . . . with HIV worldwideÂ” only 1â‹…4% [= 471,457 (obtained by substracting the WHOÂ’s cumulative total of 1999 from that of 2000)] developed AIDS in 2000, and similarly low percentages prevailed in all previous years (28). Likewise, in 1985, only 1â‹…2% of the 1 million US citizens with HIV developed AIDS (29, 30). Since an annual incidence of 1â‹…2Â–1â‹…4% of all 26 AIDS defining diseases combined is no more than the normal mortality in the US and Europe (life expectancy of 75 years), HIV must be a passenger virus.

9. A vaccine against HIV should (Â“is hopedÂ” to) prevent AIDS Â– the reason why AIDS researchers try to develop an AIDS vaccine since 1984 (31).

But, despite enormous efforts there is no such vaccine to this day (31). Moreover, since AIDS occurs by definition only in the presence of natural antibodies against HIV (Â§ 3), and since natural antibodies are so effective that no HIV is detectable in AIDS patients (see No. 1), even the hopes for a vaccine are irrational.

10. HIV, like other viruses, survives by transmission from host to host, which is said to be mediated Â“through sexual con- tactÂ”.

But, only 1 in 1000 unprotected sexual contacts transmits HIV (32Â–34), and only 1 of 275 US citizens is HIV-infec- ted (29, 30), (figure 1b). Therefore, an average un-infected US citizen needs 275,000 random Â“sexual contactsÂ” to get infected and spread HIV Â– an unlikely basis for an epidemic!

11. Â“AIDS spreads by infectionÂ” of HIV.

But, contrary to the spread of AIDS, there is no Â“spreadÂ” of HIV in the US. In the US HIV infections have remained constant at 1 million from 1985 (29) until now (30), (see also The Durban Declaration and figure 1b). By contrast, AIDS has increased from 1981 until 1992 and has decli- ned ever since (figure 1a).

12. Many of the 3 million people who annually receive blood trans- fusions in the US for life-threatening diseases (51), should have developed AIDS from HIV-infected blood donors prior to the elimination of HIV from the blood supply in 1985.

But there was no increase in AIDS-defining diseases in HIV-positive transfusion recipients in the AIDS era (52), and no AIDS-defining KaposiÂ’s sarcoma has ever been observed in millions of transfusion recipients (53).

13. Doctors are at high risk to contract AIDS from patients, HIV researchers from virus preparations, wives of HIV-positive hemophiliacs from husbands, and prostitutes from clients Â– particularly since there is no HIV vaccine.

But, in the peer-reviewed literature there is not one doctor or nurse who has ever contracted AIDS (not just HIV) from the over 816,000 AIDS patients recorded in the US in 22 years (30). Not one of over ten thousand HIV researchers has con- tracted AIDS. Wives of hemophiliacs do not get AIDS (35). And there is no AIDS-epidemic in prostitutes (36Â–38). Thus AIDS is not contagious (39, 40).

14. Viral AIDS Â– like all viral/microbial epidemics in the past (41Â–43) Â– should spread randomly in a population.

But, in the US and Europe AIDS is restricted since 1981 to two main risk groups, intravenous drug users and male homosexual drug users (Â§ 1 and 4).

15. A viral AIDS epidemic should form a classical, bell-shaped chronological curve (41Â–43), rising exponentially via virus spread and declining exponentially via natural immunity, within months (see figure 3a).

But, AIDS has been increasing slowly since 1981 for 12 years and is now declining since 1993 (figure 1a), just like a lifestyle epidemic, as for example lung cancer from smoking (figure 3b).

16. AIDS should be a pediatric epidemic now, because HIV is transmitted Â“from mother to infantÂ” at rates of 25Â–50% (44Â– 49), and because Â“34â‹…3 million people worldwideÂ” were already infected in 2000. To reduce the high maternal trans- mission rate HIV-antibody-positive pregnant mothers are treated with AZT for up to 6 months prior to birth (Â§ 4).

But, less than 1% of AIDS in the US and Europe is pediatric (30, 50). Thus HIV must be a passenger virus in new- borns.

17. Â“HIV recognizes no social, political or geographic bordersÂ” Â– just like all other viruses.

But, the presumably HIV-caused AIDS epidemics of Africa and of the US and Europe differ both clinically and epidemiologically (Â§ 1, table 2). The US/European epidemic is highly nonrandom, 80% male and restricted to abnormal risk groups, whereas the African epidemic is random.

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