HIV-1 and the aetiology of AIDS

  title={HIV-1 and the aetiology of AIDS},
  author={Martin T Schechter and Kevin J. P. Craib and Julio S. G. Montaner and Thi Nhung Le and Michael V. O’Shaughnessy and Karen A. Gelmon},
  journal={The Lancet},

HIV causes AIDS: Koch's postulates fulfilled.

HIV, AIDS, and the distortion of science.

The denialist view— based as it is on the distortion of science— is fundamentally dangerous, since it sets the stage for another wave of transmission and death.

How does HIV cause AIDS

Overall, it is increasingly evident that both the tropism and burden of HIV infection correlate closely with the manifestations of disease.

HIV-specific cytotoxic T-cells in HIV-exposed but uninfected Gambian women

This work has identified four HIV-1 and HIV-2 cross-reactive peptide epitopes, presented to CTL from HIV-infected Gambians by HLA-B35 (the most common Gambian class I HLA molecule), which may represent protective immunity against HIV infection.

AIDS Denialism and Public Health Practice

It is shown how statistics on mortality and indices such as crude death rate, life expectancy, child mortality, and population growth are consistent with the high mortality from AIDS, and the weakness of statistics from death notification, quoted by denialists are exposed.

The AIDS dilemma: drug diseases blamed on a passenger virus

It is proposed that the long-term consumption of recreational drugs and prescriptions of DNA chain-terminating and other anti-HIV drugs, cause all AIDS diseases in America and Europe that exceed their long-established, national backgrounds, i.e. <95%.

Cofactors and markers of disease progression in human immunodeficiency virus infection

The roles of the CD4 cell count and the viral load as markers of disease progression are described and the recent findings on chemokine receptors in HIV infection are discussed.

Rapid Detection of HIV-1 Subtypes in Ghana by Heteroduplex Mobility Assay

The HIV-1 CRF02_AG in Ghana has spread much more rapidly than the previously predominant subtype A over the years and the HMA is presented as a useful tool for monitoring subtype emergence and distribution in the country.

Long-term nitrite inhalant exposure and cancer risk in men who have sex with men: a prospective cohort study.

Long-term heavy popper use is associated with elevated risk of some virus-associated cancers with etiologies related to HPV, HHV-8, and EBV infections in older HIV-uninfected MSM independent of sexual behavior and immunological parameters.



AIDS epidemiology: inconsistencies with human immunodeficiency virus and with infectious disease.

  • P. Duesberg
  • Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 1991
It was concluded that American AIDS is not infectious, and it was suggested that unidentified, mostly noninfectious pathogens cause AIDS.

Human immunodeficiency virus and acquired immunodeficiency syndrome: correlation but not causation.

  • P. Duesberg
  • Medicine, Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1989
HIV is not sufficient for AIDS and that it may not even be necessary for AIDS because its activity is just as low in symptomatic carriers as in asymptomatic carriers, and the correlation between antibody to HIV and AIDS does not prove causation.

The human immunodeficiency virus: infectivity and mechanisms of pathogenesis.

Infection with the human immunodeficiency virus (HIV) results in a profound immunosuppression due predominantly to a selective depletion of helper/inducer T lymphocytes that express the receptor for

Low HIV‐1 proviral DNA burden detected by negative polymerase chain reaction in seropositive individuals correlates with slower disease progression

It is concluded that PCR can identify a group of HIV-infected people with very low levels of proviral DNA who demonstrate slower progression of the effects of HIV.

Retroviruses as carcinogens and pathogens: expectations and reality.

It has been proposed that retroviruses transform inefficiently by activating latent cellular oncogenes by for example provirus integration, which predicts diploid tumors with great diversity, because integration sites are different in each tumor.