Duesberg hypothesis

Jump to navigation Jump to search

The Duesberg hypothesis is the claim, associated with University of California, Berkeley professor Peter Duesberg, that various non-infectious factors such as recreational and pharmaceutical drug use are the cause of AIDS, and that HIV (human immunodeficiency virus) is a harmless passenger virus. The most prominent defenders of this hypothesis are Duesberg himself, biochemist and vitamin proponent David Rasnick, and journalist Celia Farber. The majority of the scientific community considers that Duesberg's arguments are the result of cherry-picking predominantly outdated scientific data[1] and selectively ignoring evidence in favour of HIV's role in AIDS.[2] There is broad scientific consensus that the Duesberg hypothesis is incorrect, and that HIV is the cause of AIDS.[3][4][5]

Role of legal and illegal drug use

Duesberg argues that there is a statistical correlation between trends in recreational drug use and trends in AIDS cases.[6] He argues that the rapid increase of AIDS cases in the 1980s corresponds to a supposed epidemic of recreational drug use in the United States and Europe during the same time frame. According to the majority of experts, this claim is not supported by epidemiologic data.[7] Duesberg's claim that recreational drug use, rather than HIV, was the cause of AIDS was specifically examined and found to be false.[8]

Duesberg has also argued that nitrite inhalants were the cause of the epidemic of Kaposi sarcoma (KS) in gay men. However, this argument has been described as an example of the fallacy of a statistical confounding effect;[9] it is now known that a herpesvirus, potentiated by HIV, is responsible for AIDS-associated KS.[10][11]

Moreover, in addition to recreational drugs, Duesberg argues that anti-HIV drugs such as zidovudine (AZT) can cause AIDS. Duesberg's claim that antiviral medication causes AIDS is regarded as disproven by the scientific community.[12]

Scientific study and rejection of Duesberg's risk-AIDS hypothesis

Several studies have specifically addressed Duesberg's claim that recreational drug abuse or sexual promiscuity were responsible for the manifestations of AIDS. An early study of his claims, published in Nature in 1993, found Duesberg's drug abuse-AIDS hypothesis to have "no basis in fact".[8]

A large prospective study followed a group of 715 homosexual men in the Vancouver, Canada area; approximately half were HIV-seropositive or became so during the follow-up period, and the remainder were HIV-seronegative. After more than 8 years of follow-up, despite similar rates of drug use, sexual contact, and other supposed risk factors in both groups, AIDS developed only in those patients who were HIV-seropositive. Similarly, CD4 counts dropped in the patients who were HIV-infected, but remained stable in the HIV-negative patients, in spite of similar rates of risk behavior.[13] The authors concluded that "the risk-AIDS hypothesis... is clearly rejected by our data", and that "...The evidence supports the hypothesis that HIV-1 has an integral role in the CD4 depletion and progressive immune dysfunction that characterise AIDS."[13]

Similarly, the Multicenter AIDS Cohort Study (MACS) and the Women's Interagency HIV Study (WIHS) — which between them observed more than 8,000 Americans — demonstrated that "...the presence of HIV infection is the only factor that is strongly and consistently associated with the conditions that define AIDS."[14]

Current AIDS definitions

Duesberg argued in 1989 that a significant number of AIDS victims had died without proof of HIV infection.[15] However, with the use of modern culture techniques and polymerase chain reaction testing, HIV can be demonstrated in virtually all patients with AIDS.[3] Since AIDS is now defined partially by the presence of HIV, Duesberg claims it is impossible by definition to offer evidence that AIDS doesn't require HIV. However, the first definitions of AIDS mentioned no cause; the addition of HIV positivity to the diagnostic criteria occurred only after a scientific consensus was established that HIV caused AIDS.

AIDS in Africa

Reported AIDS cases in Africa and other parts of the developing world, where only limited attempts are made to test for HIV infection, include people who do not belong to Duesberg's preferred risk groups of drug addicts and male homosexuals[citation needed], and it would be difficult to separate the collected data to exclude non-drug users and non-gays. Presence of HIV is not required to designate a person as having HIV, in African populations.[citation needed] In fact, Duesberg writes on his website that "There are no risk groups in Africa, like drug addicts and homosexuals."

According to Duesberg, the majority of African AIDS cases may be explained as malnutrition, parasitic infection, and poor sanitation, even though African AIDS cases have increased in the last two decades as HIV's prevalence has increased and as malnutrition and poor sanitation have declined in Africa.[citation needed]

The diseases developed by people with AIDS differ radically between African and Western populations. For example, tuberculosis is much more commonly diagnosed among AIDS patients in Africa than in Western countries, while PCP conforms to the opposite pattern.[16] The aggressive, AIDS-associated form of Kaposi's sarcoma is fairly common among heterosexuals in some parts of Africa, but is largely restricted to gay men in the USA and Europe.[17]

Duesberg's offer to infect himself

Duesberg's most radical challenge to the HIV-AIDS hypothesis is his offer to infect himself with HIV. However, he claims that it is not permissible for him to do so without the approval of the U.S. National Institutes of Health and the university that employs him. Critics regard this as a stunt, because the NIH cannot ethically give "approval" for a person to knowingly infect themselves with HIV.

Duesberg claims that retroviruses like HIV must be harmless to survive

Peter Duesberg argues that retroviruses like HIV must be harmless to survive, because after reverse transcription of their RNA to DNA, they depend on cell division to replicate. They cannot replicate in neurons, for example, because these cells do not divide (after the age of one year).[citation needed] He claims that the normal mode of proliferation of retroviruses is from mother to child, thus implying the survival of the infected mother and the child for decades.[citation needed]

This claim may be related to the fact that about 8% of the human genome is composed of harmless retroviral sequences called retrotransposons.[18] These sequences, such as the Alu sequence, are molecular fossils and can no longer form active virus particles.[19] However, the presence of these fossil sequences can influence the genome around them. For example, the gene encoding for amylase production in saliva is due to a reterotransposon inserted just upstream of the body's amylase gene.[20] The retroviral DNA's promoter sequence induces the gene to be transcribed in the mouth.

Most researchers believe that some retroviruses can cause cancer. Peter Duesberg rejects this idea.

Scientific response to the Duesberg hypothesis

The current consensus in the scientific community is that the Duesberg hypothesis has been refuted by a large and growing mass of evidence showing that causation of AIDS by HIV is clear, that virus numbers in the blood correlate with disease progression, that a plausible mechanism for HIV's action has been proposed, and that anti-HIV medication decreases mortality and opportunistic infection in people with AIDS but.[3]

In the December 9 1994 issue of Science (Vol. 266, No. 5191),[2] Duesberg's methods and claims were evaluated. The authors concluded that:

  • it is abundantly evident that HIV causes disease and death in hemophiliacs, a group generally lacking Duesberg's proposed risk factors.[21][3]
  • HIV fulfills Koch's postulates, which are one set of criteria for demonstrating a causal relationship between a microbe and a disease.[22][23]
  • the AIDS epidemic in Thailand cited by Duesberg as confirmation of his hypothesis is in fact evidence of the role of HIV in AIDS.[24]
  • According to researchers who conducted large-scale studies of AZT, the drug does not cause AIDS. Furthermore, researchers acknowledged that recreational drugs do cause immune abnormalities, though not the type of immunodeficiency seen in AIDS.[25]

Effectiveness of antiretroviral medication

The vast majority of people with AIDS have never received antiretroviral drugs, including those in developed countries prior to the licensure of AZT in 1987, and people in developing countries today where very few individuals have access to these medications.[26]

In the mid-1980s, clinical trials enrolling patients with AIDS found that AZT given as single-drug therapy conferred a modest (and short-lived) survival advantage compared to placebo. Among HIV-infected patients who had not yet developed AIDS, placebo-controlled trials found that AZT given as single-drug therapy delayed, for a year or two, the onset of AIDS-related illnesses. Significantly, long-term follow-up of these trials did not show a prolonged benefit of AZT, but also did not indicate that the drug increased disease progression or mortality. The lack of excess AIDS cases and death in the AZT arms of these placebo-controlled trials effectively counters the argument that AZT causes AIDS.[12]

Subsequent clinical trials found that patients receiving two-drug combinations had up to 50 percent improvements in time to progression to AIDS and in survival when compared to people receiving single-drug therapy. In more recent years, three-drug combination therapies have produced another 50 to 80 percent improvement in progression to AIDS and in survival when compared to two-drug regimens in clinical trials.[27] Use of potent anti-HIV combination therapies has contributed to dramatic reductions in the incidence of AIDS and AIDS-related deaths in populations where these drugs are widely available, an effect which clearly would not be seen if antiretroviral drugs caused AIDS.[28][29][30][31][32][33][34][35][36][37]

AIDS in Africa

The Duesberg hypothesis argues that AIDS in Africa is the result of poor sanitation and malnutrition, not HIV. Critics note the following facts:

  • AIDS in Africa has increased during the last two decades, in tandem with the prevalence of HIV.[38]
  • Sanitation and nutrition, on the other hand, have noticeably improved since the 1980s, when the Ethiopian famine was prominent in the news, yet AIDS case rates continued to increase.[citation needed]
  • AIDS in Africa largely kills sexually active working-age adults.[39][40]
  • The groups that have HIV are those dying from AIDS. For example, in areas where surveys show 50% of people with HIV are women, that area will show that 50% of people dying from AIDS are women. In areas where 20% of HIV+ people use recreational drugs, then 20% of the people dying from AIDS use recreational drugs.[citation needed]

Opponents claim that nearly all HIV-positive people will develop AIDS

Duesberg claims as support for his idea that many drug-free HIV+ people have not yet developed AIDS; other scientists note that many other drug-free HIV+ people have developed AIDS, and that if they wait long enough, it is very likely that nearly all of the HIV+ people will develop AIDS. Mainstream scientists also note that drug-using HIV-negative people do not seem to suffer from immune system collapse.


See also

References

  1. ↑ Galea P, Chermann JC. (1998). "HIV as the cause of AIDS and associated diseases". Genetica. 104 (2): 133–142. PMID 10220906.
  2. ↑ 2.0 2.1 Cohen J. (1994) The Duesberg phenomenon. Science 266, 1642-1644 PMID 7992043
  3. ↑ 3.0 3.1 3.2 3.3 National Institutes of Allergy and Infectious Disease Fact Sheet: The Evidence that HIV Causes AIDS. Accessed via National Institutes of Health website on March 9 2007.
  4. ↑ Fact Sheets on HIV/AIDS, from the Centers for Disease Control. Accessed March 9 2007.
  5. ↑ World Health Organization HIV and AIDS Programme, from the World Health Organization website. Accessed March 9 2007.
  6. ↑ Duesberg P, Rasnick D (1998). "The AIDS dilemma: drug diseases blamed on a passenger virus". Genetica. 104 (2): 85–132. PMID 10220905.
  7. ↑ Trends in Drug Use and the AIDS Epidemic. From the NIAID and National Institutes of Health website. Accessed 24 October 2006.
  8. ↑ 8.0 8.1 Ascher MS, Sheppard HW, Winkelstein W, Vittinghoff E (1993). "Does drug use cause AIDS?". Nature. 362 (6416): 103–4. doi:10.1038/362103a0. PMID 8095697.
  9. ↑ Morabia A (1995). "Poppers, Kaposi's sarcoma, and HIV infection: empirical example of a strong confounding effect?". Prev Med. 24 (1): 90–5. PMID 7661947.
  10. ↑ Kedes D, Operskalski E, Busch M, Kohn R, Flood J, Ganem D (1996). "The seroepidemiology of human herpesvirus 8 (Kaposi's sarcoma-associated herpesvirus): distribution of infection in KS risk groups and evidence for sexual transmission". Nat Med. 2 (8): 918–24. PMID 8705863.
  11. ↑ Martin J, Ganem D, Osmond D, Page-Shafer K, Macrae D, Kedes D (1998). "Sexual transmission and the natural history of human herpesvirus 8 infection". N Engl J Med. 338 (14): 948–54. PMID 9521982.
  12. ↑ 12.0 12.1 "AZT and AIDS". From the National Institute of Allergy and Infectious Diseases fact sheet on HIV/AIDS. Accessed March 9 2007.
  13. ↑ 13.0 13.1 Schechter M, Craib K, Gelmon K, Montaner J, Le T, O'Shaughnessy M (1993). "HIV-1 and the aetiology of AIDS". Lancet. 341 (8846): 658–9. PMID 8095571.
  14. ↑ MACS and WIHS Studies Provide Overwhelming Evidence That HIV Causes AIDS. From the National Institute of Allergy and Infectious Diseases. Accessed March 9 2007.
  15. ↑ Duesberg P (1989). "Human immunodeficiency virus and acquired immunodeficiency syndrome: correlation but not causation". Proc Natl Acad Sci U S A. 86 (3): 755–64. PMID 2644642.
  16. ↑ Cohen J. (2000) Is AIDS in Africa a distinct disease? Science 288(5474), 2153-5 PMID 10896593
  17. ↑ Chokunonga E, Levy LM, Bassett MT, Borok MZ, Mauchaza BG, Chirenje MZ, Parkin DM. (1999) Aids and cancer in Africa: the evolving epidemic in Zimbabwe. AIDS 13(18), 2583-8 PMID 10630528
  18. ↑ Mayer J, Meese E (2005). "Human endogenous retroviruses in the primate lineage and their influence on host genomes". Cytogenet. Genome Res. 110 (1–4): 448–56. PMID 16093697.
  19. ↑ Rowold DJ, Herrera RJ (2000). "Alu elements and the human genome". Genetica. 108 (1): 57–72. PMID 11145422.
  20. ↑ Ting CN, Rosenberg MP, Snow CM, Samuelson LC, Meisler MH (1992). "Endogenous retroviral sequences are required for tissue-specific expression of a human salivary amylase gene". Genes Dev. 6 (8): 1457–65. PMID 1379564.
  21. ↑ Cohen J. (1994a) Duesberg and critics agree: Hemophilia is the best test. Science 266, 1645-1646 PMID 7992044
  22. ↑ Cohen J. (1994b) Fulfilling Koch's postulates. Science 266, 1647 PMID 7992045
  23. ↑ Harden V (1992). "Koch's postulates and the etiology of AIDS: an historical perspective". Hist Philos Life Sci. 14 (2): 249–69. PMID 1342726. Full text available from National Institutes of Health website.
  24. ↑ Cohen J. (1994c) The epidemic in Thailand. Science 266, 1647 PMID 7992046
  25. ↑ Cohen J. (1994d) Could drugs, rather than a virus be the cause of AIDS? Science 266, 1648-1649 PMID 7992047
  26. ↑ UNAIDS, 2003.
  27. ↑ HHS, 2005
  28. ↑ Palella FJ Jr, Delaney KM, Moorman AC, Loveless MO, Fuhrer J, Satten GA, Aschman DJ, Holmberg SD. (1998) Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators. N. Engl. J. Med. 338, 853-860 PMID 9516219
  29. ↑ Mocroft A, Vella S, Benfield TL, Chiesi A, Miller V, Gargalianos P, d'Arminio Monforte A, Yust I, Bruun JN, Phillips AN, Lundgren JD. (1998) Changing patterns of mortality across Europe in patients infected with HIV-1. EuroSIDA Study Group. Lancet 352, 1725-1730 PMID 9848347
  30. ↑ Mocroft A, Katlama C, Johnson AM, Pradier C, Antunes F, Mulcahy F, Chiesi A, Phillips AN, Kirk O, Lundgren JD. (2000) AIDS across Europe, 1994-98: the EuroSIDA study. Lancet 356, 291-296 PMID 11071184
  31. ↑ Vittinghoff E, Scheer S, O'Malley P, Colfax G, Holmberg SD, Buchbinder SP. (1999) Combination antiretroviral therapy and recent declines in AIDS incidence and mortality. J. Infect. Dis. 179, 717-720 PMID 9952385
  32. ↑ Detels R, Munoz A, McFarlane G, Kingsley LA, Margolick JB, Giorgi J, Schrager LK, Phair JP. (1998) Effectiveness of potent antiretroviral therapy on time to AIDS and death in men with known HIV infection duration. Multicenter AIDS Cohort Study Investigators. JAMA 280, 1497-1503 PMID 9809730
  33. ↑ de Martino M, Tovo PA, Balducci M, Galli L, Gabiano C, Rezza G, Pezzotti P. (2000) Reduction in mortality with availability of antiretroviral therapy for children with perinatal HIV-1 infection. Italian Register for HIV Infection in Children and the Italian National AIDS Registry. JAMA 284, 190-197 PMID 10889592
  34. ↑ Hogg RS, Yip B, Kully C, Craib KJ, O'Shaughnessy MV, Schechter MT, Montaner JS. (1999) Improved survival among HIV-infected patients after initiation of triple-drug antiretroviral regimens. CMAJ 160, 659-665 PMID 10102000
  35. ↑ Schwarcz SK, Hsu LC, Vittinghoff E, Katz MH. (2000) Impact of protease inhibitors and other antiretroviral treatments on acquired immunodeficiency syndrome survival in San Francisco, California, 1987-1996. Am J Epidem 152, 178-185 PMID 10909955
  36. ↑ Kaplan JE, Hanson D, Dworkin MS, Frederick T, Bertolli J, Lindegren ML, Holmberg S, Jones JL. (2000) Epidemiology of human immunodeficiency virus-associated opportunistic infections in the United States in the era of highly active antiretroviral therapy. Clin Infect Dis. Suppl 1, S5-14 PMID 10770911
  37. ↑ McNaghten AD, Hanson DL, Jones JL, Dworkin MS, Ward JW. (1999) Effects of antiretroviral therapy and opportunistic illness primary chemoprophylaxis on survival after AIDS diagnosis. Adult/Adolescent Spectrum of Disease Group. AIDS 13, 1687-1695 PMID 10509570
  38. ↑ Boerma JT, Nunn AJ, Whitworth JA. (1998) Mortality impact of the AIDS epidemic: evidence from community studies in less developed countries. AIDS 12 Suppl 1, S3-14 PMID 9677185
  39. ↑ Nunn AJ, Mulder DW, Kamali A, Ruberantwari A, Kengeya-Kayondo J-F, Whitworth J. (1997) Mortality associated with HIV-1 infection over five years in a rural Ugandan population: cohort study. BMJ 315, 767-771 PMID 9345167
  40. ↑ Borgdorff MW, Barongo LR, Klokke AH, Newell JN, Senkoro KP, Velema JP, Gabone RM. (1995) HIV-1 incidence and HIV-1 associated mortality in a cohort of urban factory workers in Tanzania. Genitourin Med. 71, 212-215 PMID 7590710

External links

Sexually transmitted diseases Main Page

AIDS Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating AIDS from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

HIV Opportunistic Infections

HIV Coinfections

HIV and Pregnancy

HIV Infection in Infants

Diagnosis

Diagnostic Study of Choice

AIDS Case Definition

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Nutrition
Drug Resistance

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

HIV Vaccine

Case Studies

Case #1

Duesberg hypothesis On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Duesberg hypothesis

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Duesberg hypothesis

CDC on Duesberg hypothesis

Duesberg hypothesis in the news

Blogs on Duesberg hypothesis

Directions to Hospitals Treating AIDS

Risk calculators and risk factors for Duesberg hypothesis

Retrieved from "https://www.wikidoc.org/index.php?title=Duesberg_hypothesis&oldid=713942"