What's the truth about AIDS?

From: richard-at-cyberjournal.org

Date: 17 Nov 2004

Subject: What's the truth about AIDS?

To: newslog-at-cyberjournal.org

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http://www.virusmyth.net/aids/index.htm

      VIRUSMYTH             A growing group of bio-medical scientists claim the cause of

      AIDS is still unknown. These heretics do not believe in the

      lethal AIDS virus called HIV. They claim that the virus is

      indeed harmless.  Most of them think AIDS is also not sexually

      transmitted; it probably has toxic  causes. People die because

      they are poisoned to death by toxic antiviral drugs.  Part of

      the AIDS dissidents even question the existence of a virus

      entity. These  HIV skeptics say that the AIDS virus has never

      really been isolated, and the AIDS  tests are worthless...

           This website tells you their story.            --------------------------------------------------------

overview presentation, very good:

    http://www.virusmyth.net/aids/tour/

summary statements by doctors:

    http://www.virusmyth.net/aids/tour/step8.htm

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selected article:

http://www.virusmyth.net/aids/data/pdresim.htm

AIDS: NON-INFECTIOUS DEFICIENCIES ACQUIRED BY DRUG CONSUMPTION AND OTHER RISK FACTORS

P.H. Duesberg

Dept. of Molecular and Cell Biology; University of California, Berkeley, CA 94720 (USA)

The first 5 AIDS cases, described in 1981, were all male

homosexual drug users with pneumocystis pneumonia and acute

cytomegalovirus infections (Gottlieb et al., 1981). Since

then, over 100,000 cases of about 25 conventional diseases

including predominantly pneumonia, Kaposi's sarcoma, lymphoma,

dementia, tuberculosis, candidiasis and diarrhoea have been

recorded as AIDS diseases in the US (CDC, 1990). Over 90 %

occurred in two major risk groups (CDC, 1990), namely in 20-

to 40-year old intravenous drug users and male homosexuals who

also consume drugs (Gottlieb et al., 1981; Lauritsen and

Wilson, 1986; CDC, 1 987; Darrow et al., 1987; Haverkos and

Dougherty, 1988; Rappoport, 1988; Adams, 1989; Chaisson et

al., 1989; Weiss, S., 1989; Friedman-Kien et a/., 1990).

Because acquired immune deficiency is thought to be the common

cause of these vastly disparate diseases, they were grouped

together as the AIDS syndrome.

There are two competing hypotheses as to what causes AIDS, the

virus-AIDS and the risk-AIDS hypothesis.

The virus-AIDS hypothesis, currently held by most medical

scientists, in particular virologists, proposes that the

retrovirus HIV (human immunodeficiency virus) causes AIDS by

killing billions of T cells but only on average 8 to 10 years

after infection (Institute of Medicine, Natl. Acad. Sci.,

1986, 1988; Coffin et al., 1986; Gallo and Montagnier, 1988;

Blattner et al., 1988; Duesberg, 1989a). HIV was originally

discovered by Montagnier and co-workers in 1983 as a latent

retrovirus in AIDS patients (Barre-Sinoussi et. al., 1983).

Tracking latent viruses, like HIV, depends largely on

technology that was only developed in the 70's and 80's. Prior

to that time, a latent virus such as HIV was practically

undetectable. It is for this reason that the virus is

perceived as "new" (Gallo and Montagnier, 1988; Blattner et

al., 1988). On the basis of the virus-AIDS hypothesis, about

25 conventional diseases are now defined as AIDS if they occur

in the presence of antibody to HIV (Institute of Medicine,

Natl. Acad. Sci., 1986, 1988; CDC, 1987, 1990; Duesberg,

1989a). However, except for antibody to HIV or rare elements

of the latent virus, there is no known distinction between

conventional Kaposi's sarcoma (Friedman-Kien et al., 1990),

Iymphoma, dementia, tuberculosis, candidiasis, diarrhoea, etc.

and their AIDS counterparts.

The fact that antibody to HIV is found in the US predominantly

in AIDS risk groups, and that about 1.5 % of the 1 to 1.5

million antibody-positive Americans develop AIDS diseases

annually (Duesberg, 1989a), are cited as the primary arguments

for the virus-AIDS hypothesis (Coffin et al., 1986; Institute

of Medicine, Natl. Acad. Sci., 1986, 1988; Gallo and

Montagnier, 1988; Blattner et al., 1988). Yet a correlation,

in particular one with antibody to a virus, is not an

unambiguous argument for viral causation of a disease

(Duesberg, 1989a). Moreover, the relevance of this correlation

to the aetiology of AIDS is questionable because it is 100 %

by definition (Institute of Medicine, Natl. Acad. Sci., 1986,

1988; Duesberg, 1989a) rather than by natural coincidence

between the diseases and HIV.

In addition, a viral aetiology of AIDS is claimed based on

anecdotal cases of transmission (Institute of Medicine, Natl.

Acad. Sci., 1986, 1988; Gallo and Montagnier, 1988; Blattner

et al., 1988). It is claimed that because of infection with

HIV, antibody-positive haemophiliacs or other

antibody-positive recipients of transfusions have developed

diseases otherwise typical of their various conditions,

although these diseases appear on average only 8 to 10 years

after antiviral immunity and only in 1-3 % of them per year

(Duesberg, 1989a). Likewise it is claimed that HIV

transmission from mother to child is the reason some

antibody-positive babies have developed typical pediatric

diseases on the average 2 years after perinatal infection

(Duesberg, 1989a) (but not the diseases typical of the major

AIDS risk groups such as Kaposi's sarcoma) (Duesberg, 1988;

Beral et al., 1990; CDC, 1990). Yet there is not a single

controlled epidemiological study to confirm the postulated

viral aetiologv of AIDS transmission, comparing for example

the incidence of AlDS-like diseases in two groups of matched

haemophiliacs that differ only in antibody to HIV (Duesberg,

1989a).

Moreover, the virus-AIDS hypothesis is not compatible with

orthodox viral pathology. It is paradoxical that:

a) Unlike all other pathogenic viruses, HIV hardly infects any

cells when it is claimed to be pathogenic (Duesberg, 1987,

1988, i989a). During AIDS, < 1 in 500 lymphocytes contain a

latent HIV provirus and only 1 in 10,000 to 100,000 contain an

active provirus-just as in millions of asymptomatic carriers

(Duesberg, 1987, 1989a, 1989b; Schnittman et al., 1989).

Therefore, it is difficult to explain the loss of billions of

T cells said to be the hallmark of AIDS (Institute of

Medicine, Natl. Acad. Sci., 1986, 1988; CDC, 1987). Like the

rest of us, even viruses need to do something to get something

done.

b) In view of the claims that in vivo HIV kills T cells

directly (Baltimore and Feinberg, 1989; Ho et al., 1989) over

99 % of the few T cells that ever become infected survive

infection to become "reservoirs" of latent HIV (Schnittman et

al., 1989).

c) In view of recent claims that viraemia is necessary for

AIDS (Baltimore and Feinberg, 1989; Coombs et al., 1989; Ho et

al., 1989), the number of infected cells remains low in all

AIDS cases (Duesberg, 1990).

d) AIDS diseases-by definition (Institute of Medicine, Natl.

Acad. Sci., 1986; Coffin et al., 1986)-only occur after the

onset of antiviral immunity, a "positive" AIDS test (Duesberg,

1987, 1988, 1989a). All other viruses cause diseases primarily

before antiviral immunity when they are biochemically most

active (Evans, 1989).

e) AIDS diseases only occur after long, unpredictable latent

periods, averaging 8 to 10 years with a minimum of 2 years in

adults (Duesberg, 1989a), while all other viruses including

pathogenic retroviruses cause primary disease within weeks

after infection. Such long latent periods are particularly

paradoxical if one argues that antiviral immunity is essential

for pathogenicity (Duesberg, 1989a).

f) The same virus would take an average of 2 years to cause

diseases in children and an average of 8 to 10 years in adults

(Institute of Medicine, Natl. Acad. Sci., 1988; Duesberg,

1989a).

g) The same virus is proposed to cause neoplastic diseases

such as Kaposi's sarcomas and AIDS lymphomas as well as

necrogenic diseases such as T-cell death or AIDS dementia

(Duesberg, 1989a). This, in particular, is implausible, since

neither Kaposi's cells nor neurons are even infected by HIV

(Duesberg, 1989a). Indeed, neurons cannot be infected by HIV

because retroviruses depend on mitosis to initiate infection

(Rubin and Temin, 1958), and neurons don't divide.

h) Immune deficiency should cause neoplasms such as Kaposi's

sarcoma and lymphoma (Duesberg, 1989a). T-cell-deficient

humans or animals such as nude mice have no more tumours than

immune competent counterparts (Kinlen, 1982; Sharkey and Fogh,

1984).

i) The most common AIDS disease in the US is pneumocystis

pneumonia while the most common AIDS diseases in Africa are

slim disease, diarrhoea and fever, although Pneumocystis

carinii is ubiquitous in all humans, including Africans

(Duesberg, 1989a).

j) AIDS diseases would occur in the US to over 90 % in males,

but would be equally distributed between the sexes in Africa

if they were caused by a sexually transmitted virus introduced

into each country about 10-20 years ago (Duesberg, 1989a).

k) Among all risk groups in the US, HIV would cause Kaposi's

sarcoma almost exclusively in homosexuals (Duesberg, 1988,

1989a; Beral et al., 1990). It is also incompatible with viral

aetiology that Kaposi's sarcomas in American homosexuals with

HIV are indistinguishable from those without (Friedman-Kien et

al., 1990).

The virus-AIDS hypothesis is unproven, because (1) HIV as the

hypothetical cause of AIDS fails to meet many classical

criteria of viral pathology, (2) HIV has not been shown to

have any unconventional properties to resolve the above

paradoxa (Duesberg, 1989a), and (3) there are no controlled

epidemiological studies showing a role for HIV in AIDS. The

view that HIV is not sufficient or even not proven to be

necessary for AIDS (Duesberg, 1987, 1988, 1989a) have been

voiced by a number of scientists including: Bialy (1988);

Eigen (1989); Evans (1989; Duesberg, 1989c); Gilbert (Hall,

1988; Liversidge, 1989); Griffin (1989); Haas (1989); Holub

(1988); Root-Bernstein (1990); Rubin (1988a,b); Schwartz

(1989); Sonnabend (1989); Stewart (1989); Weiss, R. (1989) and

at least one non-scientist, Fauci's sister Denise (Fauci,

1989; Duesberg, 1989d). Moreover, Friedman-Kien et al. (1990)

and Beral et al. (1990) have now called HIV into question as a

cause of Kaposi's sarcoma, which used to be the hallmark of

AIDS in the early 80's (Beral et al., 1990) for the same

reasons I have cited above and previously (Duesberg, 1989a).

The risk-AIDS hypothesis suggests that AIDS is caused

primarily by non-infectious agents. These include psychoactive

drugs, overmedication with antibiotics (Rappoport, 1988;

Rubin, 1988a; Adams, 1989; Sonnabend, 1989) and above all AZT,

a chain terminator of DNA synthesis administered to treat HIV

infection since 1987 (Duesberg, 1989a; Farber, 1989;

Lauritsen, 1989). Consumption of psychoactive drugs is often

associated with traditional causes for immune deficiency such

as protein malnutrition and parasitic infections (Seligman et

al., 1984) and AZT is directly immunosuppressive because it is

designed to kill lymphocytes (Duesberg, 1989a; Farber, 1989;

Lauritsen, 1989). This hypothesis is compatible with views

stated by RootBernstein (1990; Rubin (1988a,b); Sonnabend

(1989); and Stewart (1989). The risk hypothesis explains:

a) Why AIDS is limited to risk groups rather than random in

the population, as would be expected from an infectious agent.

b) Why natural vaccination against HIV (a "positive AIDS

test") does not protect against AIDS.

c) The long and unpredictable latent periods between HIV

infection and AIDS, averaging 8 to 10 years in adults, as the

individual reaches a pathogenic threshold of AIDS risks. The

shorter latent periods in children averaging about 2 years

would reflect prenatal and postnatal risk factors, as 90 % of

babies with AIDS are either, born to mothers who are drug

addicts or prostitutes or both, or- are haemophiliacs

(Duesberg, 1988; CDC, l99O).

d) The enormous diversity and risk-group-specificity of AIDS

diseases in terms of the diversity of risk factors. For

example, the incidence of Kaposi's sarcoma exclusively- in

homosexuals correlates and declines directly with their

group-specific use of nitrite inhalants (Lauritsen and Wilson,

1986; Haverkos and Dougherty, 1988; Rappoport, 1988; Duesberg,

1989a; Beral et al., 1990) regardless of the presence of HIV

(Friedman-Kien et al., 1990). The nearly complete difference

between the major AIDS diseases in the US and Africa could be

explained as a consequence of drug consumption in the US and

of malnutrition and conventional parasitic infections in

Africa.

e) The paradox as to why HIV, unless an innocent bystander,

can afford to infect actively 1 in 10,000 and latently < 1 in

500 susceptible lymphocytes even in those dying from AIDS

(Duesberg, 1989a; Coombs et al., 1989; Ho et al., 1989;

Schnittman el a/., 1989).

f) The recent emergence of AIDS diseases in the US as a

function of the enormous increase during the last 10 to 20

years in the consumption of psychoactive drugs (NNICC Reports,

1978-1988; Rappoport, 1988; Adams, 1989). For instance,

cocaine consumption alone has increased 5-fold during the last

10 years in the US (NNICC Reports, 1978-1988). Indeed, about a

third of the American AIDS patients are confirmed intravenous

drug users (CDC, 1990). In addition many, perhaps most, of the

male homosexuals with AIDS appear to have used various

psychoactive drugs (Gottlieb et al., 1981; Lauritsen and

Wilson, 1986; Darrow et al., 1987; Haverkos and Dougherty,

1988; Rappoport, 1988; CDC, 1990; Adams, 1989; Friedman-Kien

et al., 1990). Together, these two risk groups represent 90 %

of the US AIDS cases (CDC, 1990). Moreover, since 1987, 20,000

antibody-positive symptomatic and asymptomatic persons in the

US (Marx, 1989) and 50,000 worldwide (Deer, 1989) have been

treated with the DNA chain terminator AZT, which is directly

immunosuppressive (Duesberg, 1989a). Thus, the use of drugs

appears to be a common denominator of most AIDS cases in the

US.

g) The preferential occurrence in the US of HIV in AIDS risk

groups can also be reconciled with the risk hypothesis. Since

HIV is not widespread in the US and also very hard to transmit

due to its chronic latency (Duesberg, 1989a), only those who

have intimate contacts with many others are likely to be

infected, as for example promiscuous homosexuals, drug addicts

sharing needles or practicing prostitution, and haemophiliacs.

Thus HIV would serve as an outstanding, but not an absolute

(Friedman-Kien et al., 1990) surrogate marker for AIDS risks

(Darrow et al., 1987; Duesberg, 1989a; Weiss, S., 1989).

It is concluded that in the US and probably in Europe, AIDS is

a collection of non-infectious deficiencies of which about 90

% are acquired by drug consumption associated with

malnutrition and parasitic infections and other specific

risks, such as chronic transfusions for treatment of

haemophilia. The 10 % of AIDS cases occurring outside the risk

groups in the US. (CDC, 1990) are consequences of the clinical

definition of AIDS, namely conventional diseases occurring in

persons accidentally infected by HIV. The African AIDS

epidemic would also appear to be the product of the

all-embracing AIDS definition, namely a widespread

heterosexual distribution of the newly detectable, dormant HIV

together with old African diseases like slim disease, fever

and diarrhoea. For example, about 10-20 % of the 30 million

Zairens carry latent HIV in Africa, but only 335 developed

AIDS in the period from 1985 to 1988 (Duesberg, 1989a). Like

nearly all retroviruses in wild animals endemic human

retroviruses are probably transmitted perinatally (Duesberg,

1989a). This would more convincingly explain the heterosexual

distribution in Africa of HIV, and hence diseases now termed

AIDS because of HIV, than theories about peculiar sexual

practices (G. Klein, 1988; Institute of Medicine, Natl. Acad.

Sci., 1988).

ACKNOWLEDGEMENT

I thank Harry Rubin and Bryan Ellison for cutical comments.

I am supported by Outstanding Investigator Grant

#5-R35-CA39915 04 from the National Cancer Institute

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Note added in proof:

The following new information in support of the risk-AIDS

hypothesis is added:

1) Recent surveys have indicated that the incidence of

AlDS-like diseases in matched risk groups is independent of

HIV up to one year after receiving HIV in general patients

(Ward et al., 1989) and probably for over 4 years in

haemophiliacs (din et al., 1989).

2) Further, it was shown that among HIV-positive mothers, drug

addiction was the only consistent risk factor for deficiencies

among newborns (Blanche et al., 1989).

3) The CDC has now retroactively revised downward the

estimates of HlV-infected persons in the US from 1-2 million

in the period of 1985-89 to 0.75 million in 1986 and about I

million in 1990 (CDC, 1990a). During the same interval, the

"latent" period from HIV to AIDS was increased from initially

three years to currently over ten years (Duesberg, 1989a).

These apparently are attempts to close the gaps that I have

pointed out between the number of AIDS cases predicted by the

virus-AIDS hypothesis and those actually recorded (Duesberg,

1989a). Moreover, the prediction of the virus-AIDS hypothesis

that, due to sexually-transmitted virus, AIDS would spread

into the heterosexual population (Institute of Medicine,

1988), has not materialized.

4) Finally, several defences of the virus-AIDS hypothesis have

failed to refute or prove erroneous the central arguments I

have raised against it. These include defences by Blattner,

Gallo and Temin (1988) / Duesberg (1988), Eigen (1989) /

Duesberg (199Oa), Evans (1989) / Duesberg (1989c), Klein

(1988)-,-Kurth (1989) / Duesberg (1989e), Velimirovic (1989) /

Duesberg (1989f), Fauci (1989) / Duesberg (1989d), Linz (1989)

/ Duesberg (1989g), and Baltimore and Feinberg (1989) /

Duesberg (1990).

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natural history of transfusion-associated infection with human

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Immunodefciency in patients with hemophilia: an underlying

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Allergy. Clin. Immunol., 83, 165.

--

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    http://www.zmag.org

    http://www.co-intelligence.org

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