VIRUSMYTH HOMEPAGE
Pharmac. & Ther. Vol. 55: 201-277, 1992
AIDS ACQUIRED BY DRUG CONSUMPTION AND OTHER NONCONTAGIOUS
RISK FACTORS
PETER
H. DUESBERG
Department of Molecular and Cell Biology, 229 Stanley Hall, University
of California at Berkeley, Berkeley, CA 94720, U.S.A.
Abstract -- The hypothesis that human immunodeficiency virus (HIV)
is a new, sexually transmitted virus that causes AIDS has been entirely
unproductive in terms of public health benefits. Moreover, it fails to
predict the epidemiology of AIDS, the annual AIDS risk and the very heterogeneous
AIDS diseases of infected persons. The correct hypothesis must explain
why: (1) AIDS includes 25 previously known diseases and two clinically
and epidemiologically very different epidemics, one in America and Europe,
the other in Africa; (2) almost all American (90%) and European (86%) AIDS
patients are males over the age of 20, while African AIDS affects both
sexes equally; (3) the annual AIDS risks of infected babies, intravenous
drug users, homosexuals who use aphrodisiacs, hemophiliacs and Africans
vary over 100-fold; (4) many AIDS patients have diseases that do not depend
on immunodeficiency, such as Kaposi's sarcoma, lymphoma, dementia and wasting;
(5) the AIDS diseases of Americans (97%) and Europeans (87%) are predetermined
by prior health risks, including long-term consumption of illicit recreational
drugs, the antiviral drug AZT and congenital deficiencies like hemophilia,
and those of Africans are Africa-specific. Both negative and positive evidence
shows that AIDS is not infectious: (1) the virus hypothesis fails all conventional
criteria of causation; (2) over 100-fold different AIDS risks in different
risk groups show that HIV is not sufficient for AIDS; (3) AIDS is only
"acquired," if at all, years after HIV is neutralized by antibodies;
(4) AIDS is new but HIV is a long-established, perinatally transmitted
retrovirus; (5) alternative explanations disprove all assumptions and anecdotal
cases cited in support of the virus hypothesis; (6) all AIDS-defining diseases
occur in matched risk groups, at the same rate, in the absence of HIV;
(7) there is no common, active microbe in all AIDS patients; (8) AIDS manifests
in unpredictable and unrelated diseases; and (9) it does not spread randomly
between the sexes in America and Europe. Based on numerous data documenting
that drugs are necessary for HIV-positives and sufficient for HIV-negatives
to develop AIDS diseases, it is proposed that all American/European AIDS
diseases, that exceed their normal background, result from recreational
and anti-HIV drugs. African AIDS is proposed to result from protein malnutrition,
poor sanitation and subsequent parasitic infections. This hypothesis resolves
all paradoxes of the virus-AIDS hypothesis. It is epidemiologically and
experimentally testable and provides a rational basis for AIDS control.
"It's too late to correct," said the Red Queen.
"When you've once said a thing, that fixes it, and you must take the
consequences."
- Lewis Carroll, Through the Looking Glass
CONTENTS
1. Virus-AIDS Hypothesis Fails to Predict Epidemiology
and Pathology of AIDS
2. Definition of AIDS
2.1. AIDS: 2 epidemics, sub-epidemics and
25 epidemic-specific diseases
2.1.1. The epidemics by case numbers, gender
and age
2.1.2. AIDS diseases
2.1.3. AIDS risk groups and risk-group specific
AIDS diseases
2.2. The HIV-AIDS hypothesis, or the definition
of AIDS
2.3. Alternative infectious theories of AIDS
3. Discrepancies Between AIDS and Infectious
Disease
3.1. Criteria of infectious and noninfectious
disease
3.2. AIDS not compatible with infectious disease
3.3. No proof for the virus-AIDS hypothesis
3.3.1. Virus hypothesis fails to meet Koch's
postulates
3.3.2. Anti-HIV immunity does not protect
against AIDS
3.3.3. Antiviral drugs do not protect against
AIDS
3.3.4. All AIDS-defining diseases occur
in the absence of HIV
3.4. Noncorrelations between HIV and AIDS
3.4.1. Only about half of American AIDS
is confirmed HIV-antibody positive
3.4.2. Antibody-positive, but virus-negative
AIDS
3.4.3. HIV: just one of many harmless microbial
markers of behavioral and clinical AIDS risks
3.4.4. Annual AIDS risks of different HIV-infected
risk groups, including babies, homosexuals, drug addicts, hemophiliacs
and Africans, differ over 100-fold
3.4.5. Specific AIDS diseases predetermined
by prior health risks
3.5. Assumptions and anecdotal cases that
appear to support the virus-AIDS hypothesis
3.5.1. HIV is presumed new because AIDS
is new
3.5.2. HIV-assumed to be sexually transmitted-depends
on perinatal transmission for survival
3.5.3. AIDS assumed to be proportional to
HIV infection
3.5.4. AIDS assumed to be homosexually transmitted
in the U.S. and Europe
3.5.5. AIDS assumed to be heterosexually
transmitted by African "lifestyle"
3.5.6. HIV claimed to be abundant in AIDS
cases
3.5.7. HIV to depend on cofactors for AIDS
3.5.8. All AIDS diseases to result from
immunodeficiency
3.5.9. HIV to induce AIDS via autoimmunity
and apoptosis
3.5.10. HIV assumed to kill T-cells
3.5.11. Antibodies assumed not to neutralize
HIV
3.5.12. HIV claimed to cause AIDS in 50%
within 10 years
3.5.13. HIV said to derive pathogenicity
from constant mutation
3.5.14. HIV assumed to cause AIDS with
genes unique among retroviruses
3.5.15. Simian retroviruses to prove that
HIV causes AIDS
3.5.16. Anecdotal AIDS cases from the general
population
3.6. Consequences of the virus-AIDS hypothesis
4. The Drug-AIDS Hypothesis
4.1. Chronological coincidence between the
drug and AIDS epidemics
4.2. Overlap between drug-use and AIDS statistics
4.3. Drug use in AIDS risk groups
4.3.1. Intravenous drug users generate a
third of all AIDS patients
4.3.2. Homosexual users of aphrodisiac drugs
generate about 60% of AIDS patients
4.3.3. Asymptomatic AZT users generate an
unknown percentage of AIDS patients
4.4. Drug use necessary for AIDS in HIV-positives
4.4.1. AIDS from recreational drugs
4.4.2. AIDS from AZT and AZT plus confounding
recreational drug use
4.5. Drug use sufficient for AIDS indicator
diseases in the absence of HIV
4.5.1. Drugs used for sexual activities
sufficient for AIDS diseases
4.5.2. Long-term intravenous drug use sufficient
for AIDS-defining diseases
4.6. Toxic effects of drugs used by AIDS patients
4.6.1. Toxicity of recreational drugs
4.6.2. Toxicity of AZT
4.7. Drug-AIDS hypothesis correctly predicts
the epidemiology and heterogeneous pathology of AIDS
4.8. Consequences of the drug-AIDS hypothesis:
Risk-specific preventions and therapies, but resentment by the virus-AIDS
establishment
5. Drugs and Other Noncontagious Risk Factors
Resolve all Paradoxes of the Virus-AIDS Hypothesis
6. Why did AIDS Science go Wrong?
6.1. The legacy of the successful germ theory:
a bias against noninfectious pathogens
6.2. Big funding and limited expertise paralyze
AIDS research
Note Added in Proof
Acknowledgements
References
VIRUSMYTH HOMEPAGE